Talk:2016 Group 5 Project

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2016 Projects: Group 1 | Group 2 | Group 3 | Group 4 | Group 5 | Group 6 | Group 7
Group Projects - Blood Cell Biology - Updated 21 April  
This year's main topic is Blood Cell Biology. Each group should discuss with group members the specific sub-topic that will be covered by their project.

Here is a list of some of the cell types (Structure and Function)

PuMed citations PuMed Central citations PuMed Central note
Note - that while full publications are available online at PuMed Central, not all these publications allow reuse. You should still always identify the copyright statement within the actual article that allows reuse. Many research labs that receive government grants are required to make their published research available on PMC, this does not mean that the publicly available copy content can be used in your projects.

Remember - No easily identifiable statement usually means that you cannot reuse.

Examples from Megakaryocyte references on PubMed Central

Embryology - content cannot be reused but a useful resource about cell development.

Histology - images these can be reused in your projects.

Group Assessment Criteria  

Group Assessment Criteria

  1. The key points relating to the topic that your group allocated are clearly described.
  2. The choice of content, headings and sub-headings, diagrams, tables, graphs show a good understanding of the topic area.
  3. Content is correctly cited and referenced.
  4. The wiki has an element of teaching at a peer level using the student's own innovative diagrams, tables or figures and/or using interesting examples or explanations.
  5. Evidence of significant research relating to basic and applied sciences that goes beyond the formal teaching activities.
  6. Relates the topic and content of the Wiki entry to learning aims of cell biology.
  7. Clearly reflects on editing/feedback from group peers and articulates how the Wiki could be improved (or not) based on peer comments/feedback. Demonstrates an ability to review own work when criticised in an open edited wiki format. Reflects on what was learned from the process of editing a peer's wiki.
  8. Evaluates own performance and that of group peers to give a rounded summary of this wiki process in terms of group effort and achievement.
  9. The content of the wiki should demonstrate to the reader that your group has researched adequately on this topic and covered the key areas necessary to inform your peers in their learning.
  10. Develops and edits the wiki entries in accordance with the above guidelines.

Group 5: User:Z5015719 | User:Z3462124 | User:Z3463953 | User:Z5017292


Project Sub-Topic

Z5015719 (talk) 18:14, 22 March 2016 (AEDT) hey guys! so does anyone have any preferences for which topic to do? I feel like they'd all be quite good, the options from red blood cell to monocyte/ macrophage look particularly good to me in terms of the marking criteria and so does the mast cell but again they all look pretty good to do. Thoughts?

Z5017292 (talk) 18:26, 22 March 2016 (AEDT)I would be happy with any of these topics really, if i had to choose then maybe mast cells would be my first choice. What is everyone else thinking?

Z5015719 (talk) 12:12, 23 March 2016 (AEDT) Mast cells sound good! so maybe we should just keep that as a tentative first option until everyone else posts what they think?

Z5017292 (talk) 12:24, 23 March 2016 (AEDT)I think that sounds like a plan.

Z5017292 (talk) 10:43, 24 March 2016 (AEDT)I've added the heading Mast Cells to our page because we needed to decide on a topic before the lab.

Z3462124 (talk) 11:06, 24 March 2016 (AEDT)

  • Cell surface specialisations
  • History of the cell and research
  • Functions

Z3462124 (talk) 11:41, 24 March 2016 (AEDT)

These two articles are review articles but they're a good place to star for background info and to find primary articles.

PMID 20176269

PMID 22577358

Z3463953 (talk)

Ok, so here is the brainstormed list of suggested subtopics: ○ Introductory paragraph ○ History § Current research § Future research ○ Morphology/structure ○ Physiology ○ Biochemistry ○ Pathology ○ CNS/ autism ○ Staining----- ○ glossary

By week 5, let's all have read the wikipedia page on mast cells, read those 4 research articles and decide which sections we're going to write!

Z5015719 (talk) 12:28, 24 March 2016 (AEDT) I just took down some notes about the marking criteria:

  • content - correctly cited and referenced: referenced source, copyright info, student image template, reference appears with the image 
  • don’t cite review article as original research- there is no new information here 
  • element of teaching to peer level 
  • citation of literature, put to date research in area (published in the last 2 years etc) - current areas of research about the cell 
  • Identify key research labs that are researching on the topic: external links that is researching something specific about the cell 
  • feedback in the group discussion (positive criticism) 
  • animations, videos (yt) (insert link), 
  • At least one image is a student drawn image 

Z5015719 (talk) 19:45, 22 April 2016 (AEST)

PMID 26976119 - this is a review article but its a good source for information on the role of mast cells in allergic diseases which is really good for our own discussion for the pathology section

PMID 12895603 - this one is also a review article, and its about the role of mast cells in asthma which gives really good background information for the pathology section as allergic diseases is a major part of mast cell function so this article is just a good source of information for this subtopic

Lab 3 Assessment

Four article summaries on one selected sub-section


Role of Mast Cells in disease and examples of diseases.

Z3462124 (talk) 11:27, 30 March 2016 (AEDT)


The aim of this article was to analyse the relationship between mast cells and the glycoslphosphatidylinositol-anchored molecule CD48, and the role of this relationship in the recognition (and immune response) of pathogenic E. coli via FimH. Malaviya demonstrated that CD48 binding to E. coli that expressed FimH could be inhibited by pretreatment of mast cells with CD48 antibodies. It was further shown that FimH-expressing E. coli effectively binds to recombinant CD48 in a cell free system and that the insertion of cDNA encoding rat CD48 into CHO (Chinese Hamster Ovary) cells resulted in CD48 acting as functional FimH receptors. Additionally, they found that pretreatment of Bone Marrow mast cells with increasing concentrations of phospholipase C resulted in a significant reduction in mast cell ability to release TNF-a (therefore decreasing neutrophil chemotaxis) after exposure to FimH-expressing E. coli. Therefore, it was shown that mast cells TNF-a response to FimH expressing bacteria is mediated by CD48 molecules which could be clinically significant in the immune response to pathogenic E. coli in the immunocompromised. [1]

This article would be useful when talking about the role of mast cells in disease as it talks about the relationship between mast cells and the FimH expressing bacteria (specifically E. coli). An understanding of the mechanisms of recognition and the immune response to bacterial pathogens is an important section of the cells role in disease. This study also explains the implications of the environment surrounding the mast cell on their ability to efficiently carry out normal functions and the effects that would have on the pathogenesis of a disease. Finally, the study also provides an explanation of the clinical significance of its findings and a possible treatment for the immunocompromised.

Mast Cell Infiltration of Colon Cancer development[2]


This study analyses the quantity of mast cell infiltration into colon tissues identified with different pathologies, including colonic polyps, well-differentiated colonic adenocarcinoma and poorly-differentitated colonic adenocarcinoma. The analysis of mast cell infiltration aimed to understand the relationship between mast cell presence and the development of colorectal cancer. Bone Marrow mast cells were co-cultured with colon cancer cells for 24-48 hours and the increase in the rate of colon cancer cell proliferation in the co-cultutred group compared to a control group indicated that colon cancer cell proliferation is significantly promoted by mast cells. It was also identified that colon chance cell migration occurred quicker in the co-cultured group where mast cells were present. After confirming that mast cell play a significant role in colon cancer cell proliferation and migration, both in vivo and in vitro, regulatory pathways of this process were analysed. It was demonstrated that mast cells promote colon cancer cell invasion and angiogenesis through MAPK/Rho-GTPase/STATs pathways. Finally, it was determined that colon tumour development can be significantly controlled via Fcε-PE40 chimeric toxin, killing mast cells without inducing degranulation and anaphylactic reaction. [3]

The major benefit and relevance of this article to the sub-section of the role of mast cells in disease, is that it demonstrates and explains an example of the negative role of mast cells in the pathogenesis of a disease. This study provides an interesting perspective on the role of mast cells in disease as they are typically thought to be cells that aid the hosts defence system rather than a stimulant of the pathogen. This article also provides an explanation of the clinical significance on their findings and suggests a possible treatment in reducing colon tutor development.


In this study, the underlying mechanisms of extracellular anti-microbal activity and mechanisms of mast cells was analysed using the bacteria S. pyogenes to exclude influence of mast cell phagocytic function. Results demonstrated that extracellular anti-microbal activity was carried out through the production of extracellular traps. It was observed that S. pyogenes growth was inhibited by human mast cells when in close proximity in a co-culture, but phagocytosis of the pathogen did not occur. Fluorescent staining of the human mast cell DNA, S. pyogenes and cathelicidin LL-37 (release by mast cells) depicted the entrapment of the pathogen in a highly defined structure containing DNA. This structure was associated with the extracellular presence of LL-37. Histones and tryptase were also recognised to be other structural components of the mast cell extracellular trap. Mast cell extracellular trap formation was demonstrated to be a result of mast cell death, a process dependent on the production of reactive oxygen species which indicated that mast cell extracellular trap formation was an active and controlled process in response to specific stimuli. This study is the first to demonstrate the formation of extracellular traps by immune cells other than neutrophils. [4]

This article is beneficial to the understanding of the role of mast cells in disease because it provides information on additional ways that mast cells influence immune response. The study outlines the formation of extra-cellular traps, a mechanism initially thought to be exclusion to neutrophils, and their role in the response to pathogens. Furthermore, it broadens the knowledge and understanding of the physiology of mast cells by presenting it as a complex cell with many mechanisms in the immune response.


The effect of histamine release, by mast cells, on the maturation of immature dendritic cells and the subsequent differentiation of naive CD4+ T cells into either Th1 or Th2 phenotypes and cytokine release was analysed in the above study. It is already known that histamine plays a major role in atopic diseases such as allergy, anaphylaxis and even asthma, however, this study demonstrates that histamines direct action on immature dendritic cells can influence the development of adaptive responses. This was supported by the observation that dendritic cells matured in a histamine rich culture polarised naive CD4+ T cells towards the Th2 phenotype. It was observed that the histamine secretion by mast cells was able to regulate the secretion of cytokines and chemokines, particularly down regulating the production of IL-12, a cytokine crucial for the development of Th1 responses. The data collected in the study also demonstrated that histamine can upregulate the expression of CD86 within dendritic cells (a component necessary for Th2 phenotype responses). Therefore, this study proposes that elevated levels of IgE and Th2 cells often present in atopic diseases could be established by a positive feedback loop of mast cell histamine release promoting Th2 phenotype differentiation and therefore IgE production, ultimately resulting in further histamine production and the positive feedback loop. [5]

Similarly to the above article, this study produces another mechanism that mast cells utilise to aid in the body's response to pathogens. This article is particularly interesting because it presents mast cells as a complex mediator of T cell maturation (towards the Th2 phenotype) through the establishment of a positive feedback loop of histamine secretion.


Z5017292 (talk) 20:08, 5 April 2016 (AEST)

Sub-Topic: Mast Cell Pathology

Article Source: Blockade of Mast Cell Activation Reduces Cutaneous Scar Formation Chen L, Schrementi ME, Ranzer MJ, Wilgus TA, DiPietro LA (2014) Blockade of Mast Cell Activation Reduces Cutaneous Scar Formation. PLoS ONE 9(1): e85226. doi: 10.1371/journal.pone.0085226

PMID 24465509

This research article explores the role of Mast cells in tissue repair, and particularly their influence on the formation of scar tissue. Mast cells are among the first cells to respond to any trauma to the body and initiate an immune response. They are present in scar tissue and the activated cells can cause excess inflammation and scar tissue to develop. This study used mice to demonstrate the effect of Mast cells on scar tissue formation. The mice were injected with a Mast cell inhibitor called disodium cromoglycate (DSCG). They were injected shortly before receiving a small 3mm incisional wound, and then given additional doses after the wounding. The results showed that the DSCG treated mice showed a reduced scar width compared to the control group. The wound breaking strength was not affected by DSCG as both the DSCG treated group and the control group displayed similar wound strength. There was less wound inflammation in the DSCG treated mice but the Mast cell inhibitor DSCG did not affect re-epithelialisation. These results suggest that Mast cell blockade has an affect on the formation of scar tissue as it reduces scar tissue formation but does not weaken the healed wound. This article is quite relevant to my topic sub-section ‘Mast cell pathology’ as it examines the role of Mast cells in tissue repair and concludes that these cells do in fact have an effect on tissue repair and scar formation. Mast cells are often seen as important in hypersensitivity reactions, so it is nice to get information on their role in other processes such as inflammation and repair.[6]

300px] Light photomicrographs of metachromatic MCs in mesenteries by toluidine blue staining. [7]

Article Source: Mast Cells Modulate Acute Toxoplasmosis in Murine Models Huang B, Huang S, Chen Y, Zheng H, Shen J, et al. (2013) Mast Cells Modulate Acute Toxoplasmosis in Murine Models. PLoS ONE 8(10): e77327. doi: 10.1371/journal.pone.0077327

PMID 24146978

This study examines the role of Mast cells in the pathogenesis of the disease Toxoplasmosis. The researchers infected mice with toxoplasma gondii and injected them with either a Mast cell inhibitor or a Mast cell activator, and then compared the levels of inflammation and parasite burden in the subjects. The results of the study revealed all of the infected mice died within 9-10 days regardless of what treatment they were given. Interestingly, the infected control mice showed severe inflammation and necrosis in the liver, but even more severe inflammation and necrosis was detected in the infected mice treated with the Mast cell activator. Conversely, the mice treated with the Mast cell inhibitor showed only mild inflammation and less necrosis. The infected mice treated with the Mast cell activator showed increased levels of parasite burden whereas the infected mice treated with the Mast cell inhibitor showed a decrease in parasite burden. These results suggest that Mast cells play an important role in parasite clearance and the inflammatory process associated with Toxoplasmosis. This indicates that Mast cells could be a potential topic for further research into controlling Toxoplasmosis.

This article is relevant to the pathology of mast cells as it demonstrates the role they play in defence against parasites. This shows that Mast cells can be quite diverse in function. It is interesting to have an article that explores the role of Mast cells in parasite defence because it shows they have a different function to the previous article that was summaries, which described their role in tissue repair. [7]

Article Source: Familial Occurrence of Systemic Mast Cell Activation Disease Molderings GJ, Haenisch B, Bogdanow M, Fimmers R, Nöthen MM (2013) Familial Occurrence of Systemic Mast Cell Activation Disease. PLoS ONE 8(9): e76241. doi: 10.1371/journal.pone.0076241

PMID 24098785

This article focuses on systemic Mast cell activation disease (MCAD) and particularly whether it can be inherited or not. Prior to this study, knowledge of familial occurrence of MCAD was very limited, but now it is thought that it may be more frequent than anticipated. The study analysed 84 patients who have MCAD and tested their first-degree relatives for the disease. The results showed that 74% of the patients had at least one relative who also had the disease. The study suggests that the prevalence of MCAD is higher among families who contain a MCAD sufferer than just the general population. This could point to a genetic link to familial occurrence as opposed to just an environmental link. This study could be a stepping stone to more research into inheritance of MCAD. This article is relevant as it explains a disorder associated with Mast cells and provides a possible explanation of how to disease is contracted. It could be interesting for the group project to include information about MCAD as it explores the effects of Mast cells on the body when they are not functioning properly. [8]

Article Source: Apoptosis and Pro-inflammatory Cytokine Response of Mast Cells Induced by Influenza A Viruses Liu B, Meng D, Wei T, Zhang S, Hu Y, et al. (2014) Apoptosis and Pro-inflammatory Cytokine Response of Mast Cells Induced by Influenza A Viruses. PLoS ONE 9(6): e100109.doi:10.1371/journal.pone.0100109

PMID 24923273

The aim of this article is to investigate the role of Mast cells in response to Influenza A infection. The article notes that Mast cells are believed to contribute to the pathogenesis of Influenza A virus, and so the study seeks to understand their contribution in further detail. The results of the study revealed that the H1N1, H5N1 and H7N2 viruses could cause mast cell apoptosis. This study was the first to uncover this information. The researchers also found that different strains of the Influenza virus caused different levels of Mast cell apoptosis. The production of the virus was impaired when the apoptosis of Mast cells was inhibited. The results of this study shed light on the role of Mast cells in defending the body against influenza, in particular how apoptosis affects the pathogenesis of influenza. This article is relevant as it demonstrates apoptosis in Mast cells, which is a defence mechanism that the cells can use when the body is under the threat of a disease. It is also interesting to have information on how Mast cells behave when under the threat of the Influenza virus because it is such a prevalent disease in the world. [9]


Structure/ morphology of mast cells

Z5015719 (talk) 22:17, 6 April 2016 (AEST)

Article Source: study of mast cells and granules from Primo Nodes using Scanning Ionic conductance microscopy

<pubmed> 26742911 </pubmed>

In this article, scanning ion conductance microscopy (SICM) is used to study the three dimensional structure of live mast cells, and the distribution of mast cell granules in each of their four developmental stages. This was done in the in the primo node (PN) of the primo vascular system from the surfaces of the large and small intestines, abdominal walls and bladder of rats, as mast cells are found to be in abundance here. Through the use of SICM, the mast cells were easily observed through the presence of their granule structures, and by the use of toludine blue stain. SICM methods were able to obtain a 3D image of these mast cells, with the surface of the cells densely covered with granules. Through this, it was able to be determined that the structure of the mast cell included 74 granules, with an average diameter of 1.2 micrometers. Upon further analysis, early stages of degranulation of the mast cell in stage 2 showed a granule-free region in the middle upper portion of the cell. In addition, the mast cell in stage 3 showed very sparse remnants of granules on the upper most parts of the cell surface. Here, SICM picked up the disintegrated boundary of the mast cell as having an appearance of laced patches, with a diameter of 1.6 micrometers. It was observed that the height of the mast cell progressively decreased with each stage, while the round shape and diameters of the granules remained the same.

This article was useful to the subtopic of mast cell structure, as it provided a detailed analysis of the structure and appearance of mast cells in their various developmental stages, with a focus on the mast cell granules during these stages. The graunles are an essential component of mast cell structure as these are secreted when mast cells are triggered, thus making it important to understand its structure. Hence, this article was useful in the research of the structure and morphology of mast cells. [10]

Article Source: A method for detailed analysis of the structure of mast cell secretory granules by negative contrast imaging

<pubmed> 26997316 </pubmed>

A 3d Image of the mast cell. Secretory granules are illustrated in white, and the nucleus and cell body are shown in the cyan and grey areas.[11]

An essential aspect of mast cell structure is the large number of secretory granules (SG) found in the cytoplasm. These elicit inflammation through molecules including histamine and serotonin. Several models suggest that a single mast cell has a large number of different types of secretory granules, all in various stages of development. Secretory granules also contain lysosomal proteins and markers such as CD63, and are hence lysosomal granules.

In order properly study the structure of mast cells, this study aims to gain insight into the structure and organisation of SGs via negative contrast imaging (NCI). Within the mast cell, organelles such as SGs are separated from the cytoplasm by a lipid bilayer, and this method uses microscopy techniques in order to visualise negatively stained organelles. These NCI techniques highlight the presence of small outlines in the perinuclear region surrounded by large, spherical shapes. NCI usage in this study also identified key structures such as the cell body, nucleoli, nuclear membrane as well as the mitochondria. The structural appearance of mast cell SGs was found to be either single elongated structures or a cluster of multiple spherical structures strung together. Experimental data indicated SGs are cylindrical in shape, and fuse along the vertical axis, highlighting polarity in structure. Further, time lapse observation during the cell cycle showed that SGs increase in abundance with cell size, but are under continuous control to maintain size distribution. This data is important as mast cell proliferation in peripheral tissues is an issue of interest in allergy treatment.

Thus, this article was beneficial in facilitating knowledge in the sub topic of mast cell morphology as it sheds light on the structure of mast cell SGs, including their organelle volume, size and number using NCI techniques. These methods can ultimately provide more information on the detailed molecular mechanisms of SG biogenesis in mast cells. [12]

Article Source: Phospholipase D2: A Pivotal Player Modulating RBL-2H3 Mast Cell Structure

<pubmed> 22344748 </pubmed>

This article examines the role of PLD2 in mast cell structure maintenance. It is thought that PLD plays a key role in mast cell degranulation, and PLD2 is essential in maintaining the structure of mast cells. The study examined if differences in PLD2 expression reflected upon alternations in morphology of the mast cells, with different cell lines being used, and was found that the inactive form of PLD2 has a dramatic effect on the morphology of these cells. The morphology of secretory granules was also determined, with these granules being heterogeneous in some cell lines include PDL2Ca, but having an electron lucid content in others. It was thus found through this study that the overexpression of the inactive form of PLD2 has a dramatic effect on the structure of mas cells, thus suggesting that the production of PA by PLD2 assists in the structural maintenance of the cytoskeleton, golgi complex as well as influencing the distribution of lysosomes and secretory granules in mast cells.

This article is hence relevant to the sub topic of mast cell structure as it highlights the specific role of PLD2 in the maintenance of the structure and morphology of the mast cell, as well as the structures within the cell. Thus, this article is beneficial as it provides a background knowledge regarding the way in which the specific structure of the cell is maintained. [13]

Article Source: NOD1 and NOD2 Interact with the Phagosome Cargo in Mast Cells: A Detailed Morphological Evidence

<pubmed> 25502289 </pubmed>

This article analyses the detailed structure of the mast cell, and in particular, the mast cell phagosome, as it has key functions in triggering the inflammatory process and has phagocytic properties. The mast cells express NOD1 and NOD2 proteins whose role is to recognize intracellular foreign components and initiate cytokine synthesis. In this study, five experiments were conducted in which mast cells were incubated with E. coli and at least 100 cells were analysed in order to determine the main morphology in each cell population. The maturation of the paghosome structure of the mast cells was also followed closely, and the outside leaflet of the mast cell plasma membrane was able to be distinguished. As structure was analysed, it was seen that many granules were interacting with the phagosome, with the phagosome membrane structure undergoing remodeling over time. It was also established that the phagosome membrane is interrupted in places in direct contact with the granule components, and these interruptions were observed at sites of granule-phagosome interaction. Additionally, NOD1 and NOD2 were found to be associated with granule surface or the granule matrix of the mast cell. The article was thus useful for this particular subtopic as it analyses the structure and morphology of the various components of the mast cell, such as the phagosome. It is beneficial to gain some perspective on the structure of the phagosome that is heavily involved in inflammatory processes, which is a key function of the mast cell. [14]


1- Mast cell activation syndrome: a newly recognized disorder with systemic clinical manifestations

Matthew J Hamilton, Jason L Hornick, Cem Akin, Mariana C Castells, Norton J Greenberger Mast cell activation syndrome: a newly recognized disorder with systemic clinical manifestations. J. Allergy Clin. Immunol.: 2011, 128(1);147-152.e2 PubMed 21621255 [edit]

File:Histology of intestine, staining for mast cells.jpg[2] Summary: People who suffer from systemic mastocytosis have clinical manifestations that are characteristic of mast cell mediator release. A similar disorder called monoclonal mast cell activation sydrome (MCAS) has an unclarified clinical manifestation. Unlike mastocytosis the patient doesn’t have abnormally high levels of mast cells (MCs), rather, the MCs they have express chemical mediators excessively. The aim of the study was to determine the clinical manifestations of MCAS and to compare it against the recently proposed diagnostic criteria. The authors of the paper ruled out clonal MC disease and found lab data indicative of MC activation. Further, the patients responded to anti-MC therapy. This was part of the classification used in this experiment to include patients as MCAS sufferers (this criteria was pre-established by previous research). The clinical manifestations and diagnostic criteria were consistent with one another. Almost all patients had abdominal pain, dermatographism or flushing. The research suggested that MCAS should have a more significant clinical profile due to its excellent response to anti-MC mediators. There were, however, some limitations such as: it was a nonblind study and there is no consensus as to a reference standard for number of mucosal mast cells in GIT.

2- John D Brannan, Johan Bood, Ahmad Alkhabaz, David Balgoma, Joceline Otis, Ingrid Delin, Barbro Dahlén, Craig E Wheelock, Parameswaran Nair, Sven-Erik Dahlén, Paul M O'Byrne The effect of omega-3 fatty acids on bronchial hyperresponsiveness, sputum eosinophilia, and mast cell mediators in asthma. Chest: 2015, 147(2);397-405 PubMed 25321659 [edit]

File:Data of PD15 (15% dec in FEV(1)) after 3 weeks of dietary Omega 3 PUFA.png[3] Summary: Poly-unsaturated fatty acids, such as some mast cell mediators, are involved in inflammation. Bronchial hyper-responsiveness (BHR) is a state of heightened sensitivity to bronchospasm that can occur as a result of mast cell mediator release in asthma and COPD. This study aimed to investigate whether dietary omega-3 PUFAs could inhibit mannitol-induced BHR. Mannitol induction of BHR mimics mast cell activation. The study was a randomize, double-blind, placebo controlled and crossover trial design. Patients suffered from asthma, did not smoke, and took omega-3s for 3 weeks. The omega 3 supplementation did not change the levels of mast cell pro-inflammatory mediator release. It is likely that it is more difficult to change the metabolic profile of mast cells than just by dietary intervention as the mast cell probably still has a significant reserve of pro-inflammatory lipids.

3- Daniel Smrz, Glenn Cruse, Michael A Beaven, Arnold Kirshenbaum, Dean D Metcalfe, Alasdair M Gilfillan Rictor negatively regulates high-affinity receptors for IgE-induced mast cell degranulation. J. Immunol.: 2014, 193(12);5924-32 PubMed 25378594 [edit]

File:MTOR and RICTOR in LAD2 cells in different environments.gif[4] Summary:

'Rapamycin-insensitive companion of mammalian target of rapamycin' (RICTOR) is a protein that regulates cell growth as a result of the presence nutrients and growth factors. This study showed that RICTOR can function as a negative regulator in igE induced mast cell degranulation, independent of other regulatory proteins like mTOR or mTOR2. They further showed at what stages in the molecular pathways the regulation took place. By analysing Ca2+ mobilisation and cytoskeletal rearrangement with confocal microscopy they were able to hypothesise that there was phosphorylation of certain proteins (LAT and PLCy1). They compared their results with a RICTOR knock-down model and found a decrease in igE induced degranulation

4- Zhuo Zhao, Hao Wang, Marina Lin, Leanne Groban GPR30 decreases cardiac chymase/angiotensin II by inhibiting local mast cell number. Biochem. Biophys. Res. Commun.: 2015, 459(1);131-6 PubMed 25712524 [edit]

File:Cardiac angiotensin (Ang) II levels in the left ventricles of sham-operated and ovariectomized (OVX) female rats.jpg[5] Summary: Estrogen seems to have protective effect on heart cells. It likely interacts via the receptor GPR30 which is expressed in the heart. Estrogen may even regulate components of hormone systems associated with the heart like the renin-angiotensin pathway. This study aimed to investigate whether the cardioprotective effects observed as a result of estrogen occur via GPR30. GPR30 has important regulatory roles in cardiac mast cell activity and proliferation. This experiment will be looking at the latter. The findings suggested that the effects of estrogen on cardiac mast cells/chymase/Ang II occur specifically through activation of GPR30 to decrease cardiac mast cell number. However, further investigations are needed for the exact mechanisms by which GPR30 affects cardiac mast cell number in vivo. Investigation in the mast cell GPR30/chymase/angII pathway could have therapeutic uses in postmenopausal women at risk of cardiovascular disease

Discussion continued

hey guys this review gives a great in depth background knowledge of mast cells and has great links to other primary research

  1. <pubmed>10393956</pubmed>
  2. <pubmed>26978404</pubmed>
  3. <pubmed>26978404</pubmed>
  4. <pubmed>18182576</pubmed>
  5. <pubmed>11748270</pubmed>
  6. <pubmed>24465509</pubmed>
  7. 7.0 7.1 <pubmed>24146978</pubmed>
  8. <pubmed>24098785</pubmed>
  9. <pubmed>24923273</pubmed>
  10. <pubmed>26742911</pubmed>
  11. <pubmed>26997316</pubmed>
  12. <pubmed>26997316</pubmed>
  13. <pubmed>22344748</pubmed>
  14. <pubmed>25502289</pubmed>