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Hydrostatic pressure induced apoptosis in PC12 cells is related to inappropriate cell-substrate adhesion


Soheil Sadri 1 (M.Sc.)
Maryam Davari Zanjani 1(M.Sc)
Mehri Azadbakht 1 (Ph.D)
Ali Amini 1(Ph.D)
Mark A.Hill 2 (Ph.D)


1- Department of Biology, Faculty of Science, Razi University, Kermanshah, Iran

2-Cell Biology Laboratory, School of Medical Sciences, University of New South Wales, Sydney, Australia

Corresponding address: Postal Code: 6714967346, Department of Biology, Faculty of Science, Razi University, Kermanshah, Iran, Ali Amini. E-mail: aamini@razi.ac.ir


Number of text pages =16

Number of legend pages =1

Number of figures =3


Abstract

Hydrostatic pressure is a crucial component of the neuronal cell’s environment and may act as a stimulus of apoptosis when pathologically increased. The mechanism relating hydrostatic pressure to neuronal apoptosis remain to be fully explained. In this study we examined the effect of hydrostatic pressure on apoptosis induction, morphology and cell-substrate interaction using the PC12 cell model. Undifferentiated and staurosporine- differentiated PC12 cells were subjected to increased hydrostatic pressure of 100 mmHg above atmospheric pressure for 2 h. Morphometric analysis of total cell body area and neurite length of cells were assessed along with dynamic processes of cell adhesion and migration. Cell death buy apoptosis was quantified using TUNEL staining. Hydrostatic pressure induced apoptosis in both undifferentiated and differentiated PC12 cells and apoptosis index in differentiated cells was more than undifferentiated cells. Morphometric analysis showed that hydrostatic pressure also reduced cell area, total neurite length, adhesion and migration ability of these cells. We suggest that the pressure-induced apoptosis in these cells was by anoikis, a cell death induced by a loss of attachment to the substrate.


Keywords: Hydrostatic pressure, Neuronal differentiation, Apoptosis, Anoikis, Staurosporine, PC12


Introduction

Cells of the various organ systems in human body are subjected to a range of mechanical forces to which they must respond. Hydrostatic pressure acting on the cell is one such fundamental environmental mechanical force. Disorders of this relationship between the cells and this mechanical force, such as when pressure varies beyond physiological limits, can lead to disease or pathological states. The sensing of mechanical forces and conversion into signals that promote a response is termed mechano-transduction. Mechanical gated ion channels and interconnected cytoskeleton-extracellular matrix (ECM) complexes are two potential mechanisms that can transduce mechanical forces to intracellular signaling [25].


The ECM provides the physical scaffold to which cells attach, however the role of ECM goes beyond physical support. In vivo cell adhesion to the ECM is mediated by cytoskeletally–linked membrane specializations called focal adhesions or focal contacts. These focal adhesions also occur in vitro between cultured cells and their underlying substrate [16]. Signal transduction through this specific adhesion is required for: survival, proliferation, differentiation, migration and in suppression of apoptosis [6]. This has been shown when loss or disruption of these cell adhesion signals induce or lead to apoptosis in an anchorage dependent manner, termed anoikis [6, 20].


Previous studies have shown that hydrostatic pressure, as a source of cell stress, acts as a stimulus for apoptosis in neuronal cell cultures [2]. The signaling mechanism(s) linking hydrostatic pressure and apoptosis in these neuronal cells remains unexplained. Such pressure related stress is also seen in the pathophysiology of neurodegenerative disorders, such as pressure-related glaucoma. The PC12 cell line [7] has been used as a model in many studies elucidating the cellular and molecular aspects of neuronal apoptosis [4, 24]. A notable characteristic of PC12 cells is that they can readily be induced to differentiate in culture with either the neurotrophic factor, nerve growth factor (NGF) [8] or the protein kinase inhibitor staurosporine [10].

This current study examined the effect on both morphology and survival of hydrostatic pressure on PC12 cells, both undifferentiated and staurosporine differentiated. This study establishes a model system to develop an understanding of the link between hydrostatic pressure and neuronal apoptosis. The results also suggest that cell-substrate adhesion is a potential step in this apoptotis.


Materials and methods

PC12 cell line were purchased from ECACC (ECACC # 88022401) and maintained in RPMI 1640 (Gibco, UK) culture medium, supplemented with 10% fetal bovine serum (Gibco, UK), 100 u/ml of penicillin and 100 mg/ml streptomycin. Cultures were incubated at 37 0 C in 5% Co2 and air.

Differentiation of undifferentiated PC12 cells was by growth in low serum medium (1%) supplemented with staurosporine (Alexis, USA) for 5 h. The optimal concentration of staurosporine for morphological differentiation without apoptosis was established by growth in a range of concentrations (110, 214, 316 and 1000 nM). Both undifferentiated undifferentiated PC12 cells and differentiated PC12 cells were exposed to hydrostatic pressure in this study, along with parallel cultures of unpressurised controls for both. In each experiment the pressure group was subjected to 100 ± 2 mmHg for 2 h within the pressure chamber. The unpressurized control cell groups were treated identically within a chamber, but without an pressure applied. The cell culture pressure chamber used in this study is an established model [2] that allows a gas mix pressurized to a constant ambient hydrostatic pressure ranging from 0 - 200±2.25 mmHg over the pressure period. After pressurization, pressure was restored to atmospheric, and the cultures plates removed from the pressure chamber for analysis.

Fixation for all cells in this study was by 4% w/v paraformaldehyde in phosphate buffered saline for 10 min at room temperature. An in situ cell death detection kit (Roche, Denmark Cat #) was used to identify the apoptotic cells by TUNEL (Terminal Uridine deoxynucleotidyl transferase dUTP Nick End Labeling) staining, following the manufacturers protocol. Briefly, all cells were fixed, permeabilized, blocked and incubated with a mixture of fluorescent labeled nucleotides on terminal deoxynucleotidy transferase (tdt) catalyzed the polymerization of labeled nucleotides to 3/0H terminals of DNA fragments. The cells were then counterstained with 10μg/ml of propidium iodide (red) at room temperature for 15 minutes and washed with PBS. A postive apoptosis control, cells induced into apoptosis by 5% ethanol treatment, were included in each assay. TUNEL positive cells were counted in 8 randomly selected fields from each culture under a fluorescent microscope (Olympus AX-70; Japan), and apoptotic index was calculated by dividing the number of apoptotic cells by the total cells. For morphological analysis both undifferentiated and differentiated cells following pressure exposure were plated (104 cells /cm2) in 24 well collagen (2%) coated culture plates. These were then grown for a range of times (0, 6, 12 and 24 h), fixed, and the morphology microscopically assessed (Motic software; Ver. 2). . Undifferentiated PC12 cell morphology could be classified as: spherical, fusiform and polygonal shape. Cell area for pressurized and unpressurised was measured separately and compared between the two groups in 6 randomly selected microscopy fields from each culture. In addition, for differentiated PC12 morphology, total neurite length was estimated by the recommended method of Ronn [19].

The adhesion assay was carried out as follows. After pressure treatment, undifferentiated and differentiated PC12 cells were detached from culture plates by trypsinization (trypsin-EDTA 0.25%, Sigma , USA) and reseeded (104 cell /cm2) in 24 well collagen (2%) coated culture plates. Following a range of time points (5, 15, 30, 60 and 120 min), non-adherent cells were gently washed out and the remaining adherent cells were fixed and counted in five randomly selected fields under phase contrast microscopy.

Cell migration was measured as described previously [12]. Briefly, cells were plated at confluent density in 6 well culture plates and pressure applied. After pressure exposure, wounding was performed using a sterile razor blade to scrap cells off the culture plate, leaving a denuded area and sharp visible demarcation line at the wounding edge. Immediately after wounding the wounded monolayer was rinsed and regions selected for migration analysis, according to the criteria described previously [12]. The cells were then incubated for 24 h with culture medium, fixed and cells that had migrated from demarcation line were counted in randomly six fields under phase contrast microscopy.

All results are expressed as a mean ± SEM from four separate experiments and were analyzed using one way analysis of variance (ANOVA) followed by Tukey’s test for comparing several doses of staurosporine for neuronal differentiation. T-test were used for the effect of hydrostatic pressure on undifferentiated and differentiated PC12 cells between pressure and control groups and comparing resistance of undifferentiated and differentiated PC12 cells in exposure to hydrostatic pressure. Statistical analysis was performed using the SPSS (Ver.16) for Windows with P value less than 0.05 considered statistically significant.

Results

Staurosporine has been previously shown to have a paradoxal dual effect dependent on its concentration. Low staurosporine concentrations induce neuronal differentiation, while high concentrations induce apoptosis. Therefore initial experiments were testing a range of staurosporine concentrations (110, 214, 316 and 1000 nM) to achieve optimal differentiation and survival. Differentiation was assessed by morphology change with neuritogenesis, the expression of neurites, as measured by neurite length. Survival, or the absence of apoptosis, was measured by TUNEL staining. In this study optimal PC12 differentiation was achieved by treatment with 214 nM staurosporine. At this concentration the average PC12 neurite length was 153 ± 15µm. Both lower and higher staurosporine concentrations were considered suboptimal. Differentiation, as determined by neuritogenesis, for each concentration is shown with average neurite length: 110 nM, 44 ± 9.3 µm; 316nM, 104 ± 10 µm; 1000 nM, 16 ± 9.6 µm. Apoptosis, as detected by TUNEL, for each concentration is shown with the apoptotic index: 110 nM, 4 ± 0.3, 214 nM, 4 ± 0.8, 316 nM, 8 ± 1 and 1000 nM, 16 ± 1.1. From both these results it was determined that staurosporine treatment at 214nM was optimal for neuronal differentiation with minimal apoptosis induction (Fig.1, P<0.05, ANOVA).

Hydrostatic pressure was found to induce apoptosis in both undifferentiated and differentiated PC12 cells. PC12 cells displayed characteristic features of apoptosis by visual inspection with phase contrast and fluorescent microscopy. The apoptotic PC12 cells exhibited bright labeling of fragmented nuclear DNA by TUNEL staining. The apoptotic index for PC12 cells in pressure groups was undifferentiated 15.0 ± 0.8 and differentiated 24.4 ± 1.2, in comparison with 3.5 ± 0.6 and 3.0 ± 0.5 in respective control groups (Fig.2, P<0.05, T-test).

Hydrostatic pressure changed shape of undifferentiated cells in all three mentioned forms. Cell area of undifferentiated cells in 0, 6, 12 and 24h was 817 ± 32, 653 ± 31, 708 ± 15 µm2 and 685 ± 28 in pressure group and 1050 ± 38, 839 ± 34, 805 ± 29 and 805 ± 33 µm2 in control group respectively, that showed statistically difference in pressure group compared to control group (Fig.3A, P<0.05, T-test).

Differentiated cells neuritogenesis at different timepoints (0, 6, 12 and 24 h) was assessed by morphometery. These cells displayed retraction of neurites and reduction in the total neurite length. In the pressure group the total neurite length at these time points was 134 ± 7.7, 132 ± 5.7, 124 ± 6.7 and 123 ± 9.0 µm respectively. In the control group, total neurie length was 176 ± 13.2, 185 ± 7.8, 196 ± 7.5 and 196 ± 7.8 µm respectively. Neuritogenesis between pressure and control groups were statistically different at all time points (Fig.3a, P<0.05, T-test).

The effects of hydrostatic pressure on cell-substrate adhesion and migration assay in these experiments are shown in Figure 3. Hydrostatic pressure treatment reduced number of adherent cells at all time points in both undifferentiated and differentiated PC12 cells (Fig.3 B). The results also showed a statistical difference between undifferentiated and differentiated PC12 cell populations (Fig.3 B and b, P<0.05, T-test).

The migration assay showed that hydrostatic pressure also decreased number of migrated cells from demarcation line in both undifferentiated and differentiated cells (Fig.3 C and c, P<0.05, T-test). Differentiated PC12 cells also showed a greater susceptibility to hydrostatic pressure in comparison with undifferentiated cells in aspect of cell adhesion and migration (P<0.05, T-test).


Discussion

This current study identified an induced apoptosis in both undifferentiated and differentiated PC12 cells following expose to hydrostatic pressure. Apoptosis in the differentiated PC12 cell population was more pronounced than in the undifferentiated PC12 population, as shown in other studies [11, 14]. Differentiation of PC12 cells leads to significant cytoskeletal reorganization and application of hydrostatic pressure to these cells can also result in changes to cytoskeletal architecture [18]. The PC12 cell line was used in this study in both undifferentiated and neural differentiated forms. PC12 cells that were treated with NGF and staurosporine stop dividing and differentiate, as indicating morphologically by extension of neurites. Differentiation by NGF treatment has been shown to enhance cellular antioxidant capacity [15, 21] and afford protection against oxidative challenge [4]. There is no experimental data that suggests staurosporine leads to an alteration of antioxidant levels, but we cannot exclude the possibility that this may also occur with any differentiation stimulus.

Staurosporine has dose-dependent effects ranging from neuronal differentiation to apoptosis induction [3, 17]. We examined staurosporine concentrations used in neuronal differentiation from other studies [5, 10] and some additional levels. Our results showed, optimal PC12 cell differentiation with 214 nM determined by longest neurite growth and with minimal apoptosis induction. This optimal concentration was therefore used for hydrostatic pressure study.

Previous studies that influenced hydrostatic pressure on neuronal cells showed that hydrostatic pressure induced apoptosis in neuronal cells. Agar et al. initially showed that neuronal cells subjected to elevated hydrostatic pressure condition of 100 mmHg in an in vitro system undergo apoptosis [1, 2]. This hydrostatic pressure level corresponds levels seen in acute glaucoma with resultant neuronal loss from the retina. Our study confirmed by TUNEL staining, apoptosis induction in both undifferentiated and differentiated PC12 cells after exposure to hydrostatic pressure. The effect was more significant in differentiated than undifferentiated PC12 cells. These findings differ from other PC12 undifferentiated/differentiated comparisons following exposure to different stresses, such as oxidative challenge and H2O2 treatment [4, 24]. These other studies show a greater susceptibility in undifferentiated PC12 cells than in differentiated cells. The difference between the current study and these other studies may relate to the methodology of differentiation and the type of stress applied to the cell. For example, NGF has been shown to be both an anti-apoptotic and antioxidant effect [4, 21].

In our earlier studies [1, 26] the mechanism whereby hydrostatic pressure triggers apoptosis was undetermined. There have been several postulated mechanisms as too how hydrostatic pressure may exert its effect on neuronal systems. Such mechanisms include trans-membrane ion fluxes [23] and membrane bound mechanosensitive ion channels [13]. No study had previously considered an effect mediated by cell-ECM interaction as having a possible role in mechano-transduction and cell death induction.

Neuronal cells usually need to attach underlying ECM to grow; spread, undergo neurite growth and for collective morphological stability [22]. These activities are modulated by various influences such as biochemical activity at cell-substrate adhesion and trophic factor effects. Cell adhesion and interactions between cell-substrate plays central role in a variety of biological phenomenon. This is integrated or coupled to the cell cytoskeleton through focal adhesions, which also provide a means for mediating mechano-sensivity and signal transduction [22]. This current study would suggest that hydrostatic pressure alters cell-substrate interaction and links to signaling that can induce apoptosis in neuronal cells.

Gue et al demonstrated for the first time apoptosis that occurred in their rat glaucoma model induced by degradation of the extracellular matrix protein laminin, as an ECM component at retina site, in response to intra ocular pressure exposure [9]. They suggested this degradation of laminin occurred in glaucoma, leading to the interruption of cell to ECM communication making the neuron more susceptible to apoptosis [9]. Our collagen substrate would contain little laminin so this suggested mechanism would not be directly applicable to our study, though it is an alteration of neuronal adhesion. Their study focused on the effect of hydrostatic pressure elevation on degradation of laminin as an essential ECM component. Our study focused on the influence of hydrostatic pressure elevation on the cell substrate adhesion and the cell’s ability to receive survival signals that suppress apoptosis. Our results showed cells began to adhere 5 min after replating and the number of adherent cells to the substrate decreased in both undifferentiated and differentiated pressure groups at all times over 120 min, that adherent cells were counted.


Further investigation of cell-substrate interaction was assessed by a migration assay. Our results showed that, the number of migrated cells from demarcation line decreased in the pressure group for both undifferentiated and differentiated PC12 cells. This may be a result of decreased in assemble and disassemble of focal contacts and collectively inappropriate cell-substrate interactions. In addition differentiated cells showed more susceptibility in adhesion and migration ability in comparison to undifferentiated cells.

In conclusion, although some evidence indicates that apoptotic cell death can be triggered by many different environmental elements; our experiments provide evidence that elevated hydrostatic pressure itself induced apoptosis in PC12 cells as a result of disruption in cell-substrate adhesion. Further study of integrins and their related adhesion proteins, such as focal adhesion kinases, may better link the effect of hydrostatic pressure to anoikis induction in neuronal cells.


References

[1] A. Agar, Sh. Li, N. Agarwal, M. Coroneo, M. Hill, Retinal ganglion cell line apoptosis induced by hydrostatic pressure, Brain Res.1086 (2006) 191-200.

[2] A. Agar, S. Yip, M. Hill, M. Coroneo, Pressure related apoptosis in neuronal cell lines, J. Neurosci. Res.60 (2000) 495-503.

[3] M. Deshmukh, E. Johnson, Staurosporine-induced neuronal death: multiple mechanisms and methodological implications, Cell Death Differ. 3 (2000) 250-261.

[4] E. Ekshyyan, T. Aw, Decreased susceptibility of differentiated PC12 cells to oxidative challenge: relationship to cellular redox and expression of apoptotic protease activator factor-1, Cell Death Differ. 2 (2005) 1066-1077.

[5] L. Frassetto, C. Schlieve, C. Lieven, A. Amy, M. Jones, N. Agarwal, L. Levin, Kinase- dependent differentiation of a retinal ganglion cell precursor, Invest. Ophthalmol. Visual Sci. 47 (2006) 427-38.

[6] S. Frisch, R. Screaton, Anoikis mechanisms, Curr. Opin. Cell Biol. 13 (2001) 555–562.

[7] L. Greene, A. Tischler, Establishment of a noradrenergic clonal line of rat adrenal pheochromocytoma cells which respond to nerve growth factor, Nat. Acid. Sci. 73 (1976) 2424- 2428.

[8] L. Greene, NGF prevents the death and stimulates the neuronal differentiation of clonal PC12 cells in serum-free medium, J. Cell Biol.78 (1978) 747–755.

[9] L. Guo, S. Moss, R. Alexander, R. Ali, F. Fitzke, M. Cordeiro, Retinal ganglion cell apoptosis in glaucoma is related to intraocular pressure effects on ECM, Invest. Ophthalmol. Visual. Sci. 46 (2005) 175–182.

[10] S. Hashimoto, A. Hagino, Staurosporinr induced neurite outgrowth in PC12 cells, Exp. Cell Res. 184 (1989) 351– 359.

[11] J. Hong, K. Noh, Y. Yoo, S. Choi, S. Park, Y. Kim, J. Chung, Iron promotes the survival and neurite extension of serum-starved PC12 cells in the presence of NGF by enhancing cell attachment, Mol. Cells 15 (2003) 10–19.

[12] J. Irving, P. Lala, Functional role of cell surface integrins on human trophoblast cell migration: regulation by TGF-b, IGF-II, and IGFBP-1, Exp. Cell Res. 217 (1995) 419-427.

[13] L. Islas, H. Pasantes-Morales, J. Sanchez, Characterization of stretch activated ion channels in cultured astrocytes, Glia 8 (1993) 87–96.

[14] M. Kwon, S. Seo, H. Chun, J. Chung, I. Chung, K. Hur, Dual effect of NGF on cell death of PC12 cells Induced by serum deprivation, Mol. Cells 13 (2002) 167–174.

[15] H. Liu, R. Nowak, W. Chao, K. Bloch, Nerve growth factor induces anti-apoptotic heme oxygenase-1 in rat pheochromocytoma (PC12) cells, J. Neurochem. 86 (2003) 1553–1563.

[16] V. Petit, J. Thiery, Focal adhesions: structure and dynamics, Biol. Cell 92 (2000) 477-494.

[17] D. Rasouly, E. Rahamim, L. Ringel, I. Ginzburg, C. Muarakata, Y.Matsuda, P. Lazarovici, Neurites induced by staurosporine in PC12 cells are resistant to colchicine and express high levels of tau proteins, Mol. Pharmaco. 45 (1993) 29-35.

[18] G. Ronald, J. Wilson, E. Judy, S. Zimmerman, A. Zimmerman, Hydrostatic pressure induced changes in the cytoarchitechture of PC12 cells, Cell Biol. Int. 7 (2001) 649–665.

[19] L. Ronn, I. Ralets, B. Hartz, M. Bech, A. Berezin, V. Berezin, A. Moller, E. Bock, A simple procedure for quantification of neurite outgrowth based on stereologicalprinciples, J. Neurosci. Method 100 (2000) 25-32.

[20] E. Ruoslahti, J. Reed, Anchorage dependence, integrins and apoptosis, Cell 77 (1994) 477-478.

[21] D. Sampath, G. Jackson, K. Werrbach-Perez, J. Perez-Polo, Effects of nerve growth factor on glutathione peroxidase and catalase in PC12 cells, J. Neurochem. 62 (1994) 2476–2479

[22] R. Seidenfaden, A. Krauter, H. Hildebrandt, The neural cell adhesion molecule (NCAM) regulates neuritogenesis by multiple mechanisms of interaction, Neurochem. Int. 49 (2006) 1-11.

[23] A. Southan, K. Wann, Effects of high helium pressure on intracellular and field potential responses in the CA1 region of the in vitro rat hippocampus, Eur. J. Neurosci. 8 (1996) 2571–2581.

[24] Y. Sung, C. Cheng, C. Chen, H. Huang, F. Huang, P. Wu, M. Shiao, J. Tsay, Distinct mechanisms account for beta-amyloid toxicity in PC12 and differentiated PC12 neuronal cells, J. Biomed. Sci. 10 (2003) 379- 288.

[25] J. Tan, F. Kalapesi, M. Coroneo, Mechanosensitivity and the eye: cells coping with the pressure, Br. J. Opht. 90 (2005) 383- 388.

[26] G. Tezel, M. Wax, Increased production of TNF-α by glial cells exposed to simulated ischemia or elevated hydrostatic pressure induced apoptosis in co-cultured retinal ganglion cells, J. Neurosci. 23 (2000) 8693- 8700.


Figure Legends

Figure 1- The dose-dependent manner of staurosporine to neuronal differentiation or apoptosis induction in PC12 cells. (A, a) Treatment with 110 nM does not differentiate PC12 cells into mature neurons without apoptosis induction shown with TUNEL staining. (B, b) Treatment with 214 nM was the optimal dose of staurosporine to differentiate PC12 cells into mature neurons without apoptosis induction. (C, c) Treatment with 316 nM differentiate PC12 cells into mature neurons but also induced apoptosis. (D, d) Treatment with 1000 nM showed damaged feature and high apoptotic cells. Scale bar = 40 µm


Figure 2- Morphological investigation of apoptosis in undifferentiated and differentiated PC12 cells after exposure to hydrostatic pressure. Phase contrast microscope image of undifferentiated and differentiated PC12 cells in control (A, C) and pressure groups (B, D). Fluorescent microscopy images of TUNEL staining in control (a, c) and pressure groups (b, d) corresponded to PC12 cells seen in phase contrast microscope image. This figure showed hydrostatic pressure induced apoptosis in both undifferentiated and differentiated PC12 cells as identified by DNA fragmentation, chromatin condensation, retraction of neuronal process and cell shrinkage (arrows). Scale bar = 40 µm


Figure 3- Quantitative analysis of hydrostatic pressure effect on morphology, adhesion and migration of undifferentiated and differentiated PC12 cells. (A) Hydrostatic pressure led to cell rounding and a statistically significantly decreased undifferentiated cells area and caused neurite retraction and statistically significant decrease in total neurite length in differentiated cells (a). A time course adhesion assay showed hydrostatic pressure statistically significantly decreased the number of adherent cells to substrate in undifferentiated (B) and differentiated cells (b). Migration assay of undifferentiated and differentiated PC12 cells 24 h after wounding revealed that hydrostatic pressure significantly decreased number of migrated cells from demarcation line in undifferentiated (C) and differentiated cells(c). * Compared to control group.

Reference List

Template:Reflist

  1. Template:Cite journal
  2. Hill MA. Early human development. Clin Obstet Gynecol. 2007 Mar;50(1):2-9. PMID:17304021

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This is where your individual assignment will live. You can also use this page for any other Cell Biology topics or resources you use in the current course. I would also appreciate any feedback from the lecture materials as shown in Comments.


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Notes

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Group 1 Meiosis

Group 1 Meiosis

Group 2 Cell Death - Apoptosis

Group 2 Cell Death - Apoptosis

Group 3 Cell Division

Group 3 Cell Division

Group 4 Trk Receptors

Group 4 Trk Receptors

Group 5 The Cell Cycle

Group 5 The Cell Cycle

Group 6 Golgi Apparatus

Group 6 Golgi Apparatus

Group 7 Mitochondria

Group 7 Mitochondria

Group 8 Cell Death - Necrosis

Group 8 Cell Death - Necrosis

Group 9 Nucleus

Group 9 Nucleus

Group 10 Cell Shape

Group 10 Cell Shape

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