Difference between revisions of "2016 Group 5 Project"

From CellBiology
(Mast Cell)
(Pathology)
Line 50: Line 50:
  
 
==Pathology==
 
==Pathology==
 +
===Role of mast cells in parathyroid bone disease===
 +
 +
(draft)
 +
 +
An increased number of mast cells in the bone marrow can be linked with parathyroid bone disease, most common of which being chronic hyperparathyroidism (HPT). Those suffering from HPT have a disturbed immune function, and mast cells play a major role in innate immunity. Parathyroid hormone (PTH) significantly increases the number of mast cells in those with HPT. There is a 5-fold increase in bone marrow mast cells in those with HPT as compared to the controls. Elevated levels of PTH increase migration of preoestoblastic fibroblasts to the bone surface, and while these generally differentiate into osteoblasts, the increased PTH levels cause terminal differentiation to be impaired. The accumulation of mast cells on bone surfaces as a response to elevated PTH levels lead to this PTH-induced peritrabcular fibrosis, and cause the excessive recruitment of fibroblasts on bone surfaces.  An increase in kit- ligand expression causes the build up of mast cells, as it is a potent chemotactic factor for these mast cells. Combined with an increased PDFG-A gene expression, these peritrabcular mast cells promote fibrosis, ultimately leading to bone disease.
 +
 +
<pubmed>20200965</pubmed><ref><pubmed>20200965</pubmed></ref>

Revision as of 23:33, 23 April 2016

2016 Projects: Group 1 | Group 2 | Group 3 | Group 4 | Group 5 | Group 6 | Group 7

Mast Cell

Introduction

History

Physiology

Structure

receptors, microscopy

Function

multifunctional purpose (don't have to go into too much detail -> more depth in following sections

Differentiation

pg700 Da silva et al


Degranulation/biogenesis

This is different to activation in that it's how the biogenesis of the mediators occurs, not how an antigen triggers the degranulation. pg 4 moon et al

Mediators

706, de silva

Activation

to read:

<pubmed>25062998</pubmed> <pubmed>25452755</pubmed> <pubmed>12592295</pubmed>


<pubmed>22561833</pubmed> review on igE interactions: http://www.nature.com/nm/journal/v18/n5/full/nm.2755.html

<pubmed>21333342</pubmed> autophagy: http://www.sciencedirect.com/science/article/pii/S0091674910030381

<pubmed>3251560</pubmed> http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251560/

http://onlinelibrary.wiley.com/doi/10.1196/annals.1392.024/abstract


http://www.karger.com/Article/FullText/337800

<pubmed>22627374</pubmed>

Pathology

Role of mast cells in parathyroid bone disease

(draft)

An increased number of mast cells in the bone marrow can be linked with parathyroid bone disease, most common of which being chronic hyperparathyroidism (HPT). Those suffering from HPT have a disturbed immune function, and mast cells play a major role in innate immunity. Parathyroid hormone (PTH) significantly increases the number of mast cells in those with HPT. There is a 5-fold increase in bone marrow mast cells in those with HPT as compared to the controls. Elevated levels of PTH increase migration of preoestoblastic fibroblasts to the bone surface, and while these generally differentiate into osteoblasts, the increased PTH levels cause terminal differentiation to be impaired. The accumulation of mast cells on bone surfaces as a response to elevated PTH levels lead to this PTH-induced peritrabcular fibrosis, and cause the excessive recruitment of fibroblasts on bone surfaces. An increase in kit- ligand expression causes the build up of mast cells, as it is a potent chemotactic factor for these mast cells. Combined with an increased PDFG-A gene expression, these peritrabcular mast cells promote fibrosis, ultimately leading to bone disease.

<pubmed>20200965</pubmed>[1]

  1. <pubmed>20200965</pubmed>