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MiR-132 controls pancreatic beta cell proliferation and survival through Pten/Akt/Foxo3 signaling

Mziaut, Hassan, Henniger, Georg, Ganss, Katharina, Hempel, Sebastian, Wolk, Steffen, McChord, Johanna, Chowdhury, Kamal, Ravassard, Philippe, Knoch, Klaus-Peter, Krautz, Christian, Weitz, Jürgen, Grützmann, Robert, Pilarsky, Christian, Solimena, Michele, Kersting, Stephan·2020·Molecular Metabolism
DOI 10.1016/j.molmet.2019.11.012PMC PMC6928290
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Figure 1 Quantification of BrdU+cells in islets of partially pancreatectomized mice. (A) Overview of the experimental design. (B) A tissue section of the remnant pancreas excised 1 week after partial pancreatectomy stained with cresyl violet to reveal the islet core. The tissue was labeled with DAPI (green) and anti-BrdU antibodies (black) to detect the cell nuclei and replicating cells, respectively. (C) Enrichment of beta cell-specific markers shown by Q-PCR of mRNA extracted from laser capture microdissected islets. (D) Percentage of BrdU+ cells in the islet cores. The analysis included 7 mice, of which 4 were sham-operated and 3 were partially pancreatectomized. 40 slices/group were counted for BrdU+ cells. *p < 0.05.
Figure 1 Quantification of BrdU+cells in islets of partially pancreatectomized mice. (A) Overview of the experimental design. (B) A tissue section of the remnant pancreas excised 1 week after partial pancreatectomy stained with cresyl violet to reveal the islet core. The tissue was labeled with DAPI (green) and anti-BrdU antibodies (black) to detect the cell nuclei and replicating cells, respectively. (C) Enrichment of beta cell-specific markers shown by Q-PCR of mRNA extracted from laser capture microdissected islets. (D) Percentage of BrdU+ cells in the islet cores. The analysis included 7 mice, of which 4 were sham-operated and 3 were partially pancreatectomized. 40 slices/group were counted for BrdU+ cells. *p < 0.05.CC BY-NC-ND · PubMed Central
Figure 2 MiR-132 regulates the proliferation and caspase levels in MIN6 cells. (A) Levels of miR-132 in MIN6 cells treated with control (white bar) or miR-132 (black bar) siRNA as determined by RT-PCR. (B-C) Representative confocal images of BrdU+ cells (green) in MIN6 cells treated with control (B) or miR-132 (C) siRNA. (D) Number of BrdU+ in control vs miR-132 depleted MIN6 cells counted from images as in (B-C). (E) Representative immunoblots for pro- and cleaved caspase-9, cleaved caspase-3, and γ-tubulin as loading controls in extracts of MIN6 cells treated with control or miR-132 siRNA. (F) Densitometric quantification of immunoblots as in (E). White bars: control siRNA-treated cells; black bars: miR-132 siRNA-treated cells. (G) Expression levels of miR-132 in MIN6 cells transduced with adenovirus vectors for the co-expression of miR-132 and eGFP (black bar) or eGFP alone (white bar) as detected by RT-PCR. (H-I) Representative confocal images of BrdU+ (red) and eGFP+ (green) MIN6 cells transduced with adenovirus vectors for the co-expression of miR-132 and eGFP (i) or eGFP alone. Nuclei were detected with DAPI (blue). (J) Number of BrdU+ and GFP+ cells normalized to GFP+ cells in MIN6 cells transduced with eGFP (white bars) or miR-132 and eGFP (black bars) counted from images as in (H-I). (K) Representative immunoblots for pro- and cleaved caspase-9, cleaved caspase-3, and γ-tubulin as loading controls in extracts of MIN6 cells transduced with adenovirus vectors for the co-expression of miR-132 and eGFP or eGFP alone. (L) Densitometric quantification of immunoblots as in (K). (M) caspase-3/7 enzymatic activity was assayed by measuring the cleavage of Z-DEVD-R110 substrate via spectrophotometry as described in the materials and methods section. (N) Expression of procaspase-9 mRNA in MIN6 cells overexpressing miR-132 (white bar) and eGFP (black bar) as measured by RT-PCR. n = 3.
Figure 2 MiR-132 regulates the proliferation and caspase levels in MIN6 cells. (A) Levels of miR-132 in MIN6 cells treated with control (white bar) or miR-132 (black bar) siRNA as determined by RT-PCR. (B-C) Representative confocal images of BrdU+ cells (green) in MIN6 cells treated with control (B) or miR-132 (C) siRNA. (D) Number of BrdU+ in control vs miR-132 depleted MIN6 cells counted from images as in (B-C). (E) Representative immunoblots for pro- and cleaved caspase-9, cleaved caspase-3, and γ-tubulin as loading controls in extracts of MIN6 cells treated with control or miR-132 siRNA. (F) Densitometric quantification of immunoblots as in (E). White bars: control siRNA-treated cells; black bars: miR-132 siRNA-treated cells. (G) Expression levels of miR-132 in MIN6 cells transduced with adenovirus vectors for the co-expression of miR-132 and eGFP (black bar) or eGFP alone (white bar) as detected by RT-PCR. (H-I) Representative confocal images of BrdU+ (red) and eGFP+ (green) MIN6 cells transduced with adenovirus vectors for the co-expression of miR-132 and eGFP (i) or eGFP alone. Nuclei were detected with DAPI (blue). (J) Number of BrdU+ and GFP+ cells normalized to GFP+ cells in MIN6 cells transduced with eGFP (white bars) or miR-132 and eGFP (black bars) counted from images as in (H-I). (K) Representative immunoblots for pro- and cleaved caspase-9, cleaved caspase-3, and γ-tubulin as loading controls in extracts of MIN6 cells transduced with adenovirus vectors for the co-expression of miR-132 and eGFP or eGFP alone. (L) Densitometric quantification of immunoblots as in (K). (M) caspase-3/7 enzymatic activity was assayed by measuring the cleavage of Z-DEVD-R110 substrate via spectrophotometry as described in the materials and methods section. (N) Expression of procaspase-9 mRNA in MIN6 cells overexpressing miR-132 (white bar) and eGFP (black bar) as measured by RT-PCR. n = 3.CC BY-NC-ND · PubMed Central
Figure 3 Effect of miR-132 on beta cell proliferation in EndoC-βH1 cells. (A–D) Representative confocal images of BrdU+ (red) and eGFP+ (green) in EndoC-βH1 cells transduced with adenovirus vectors for control eGFP (A and C) or miR-132-eGFP (B and D) expression either in 1.4 mM DMSO (A and B) or 10 μM harmine (C and D). Nuclei were detected with DAPI (blue). (E) BrdU+ and GFP+ EndoC-βH1 cells normalized to GFP+ cells in control or miR-132 overexpressing cells treated as described in (A-D). (F) Mean number of DAPI+ cells of EndoC-βH1 cells/field transduced as described in (A–D). White bars: cells transduced with CMV-eGFP adenovirus vector; black bars: cells transduced with CMV-miR-132/eGFP adenovirus vector. (G) Relative miR-132 level in EndoC-βH1 cells treated with 1.4 mM DMSO or 10 μM harmine. Data shown in (A–D) were collected from 15 to 20 images with 1,000–4,000 cells for each condition. Scale bars in (A–D) = 50 μm *p < 0.05, **p < 0.01, **p < 0.001.
Figure 3 Effect of miR-132 on beta cell proliferation in EndoC-βH1 cells. (A–D) Representative confocal images of BrdU+ (red) and eGFP+ (green) in EndoC-βH1 cells transduced with adenovirus vectors for control eGFP (A and C) or miR-132-eGFP (B and D) expression either in 1.4 mM DMSO (A and B) or 10 μM harmine (C and D). Nuclei were detected with DAPI (blue). (E) BrdU+ and GFP+ EndoC-βH1 cells normalized to GFP+ cells in control or miR-132 overexpressing cells treated as described in (A-D). (F) Mean number of DAPI+ cells of EndoC-βH1 cells/field transduced as described in (A–D). White bars: cells transduced with CMV-eGFP adenovirus vector; black bars: cells transduced with CMV-miR-132/eGFP adenovirus vector. (G) Relative miR-132 level in EndoC-βH1 cells treated with 1.4 mM DMSO or 10 μM harmine. Data shown in (A–D) were collected from 15 to 20 images with 1,000–4,000 cells for each condition. Scale bars in (A–D) = 50 μm *p < 0.05, **p < 0.01, **p < 0.001.CC BY-NC-ND · PubMed Central
Figure 4 Identification and validation of miR-132 target genes in MIN6 cells. (A) Venn diagram showing the number of down- and upregulated genes in MIN6 cells transduced with CMV-miR-132/eGFP adenovirus vector compared to MIN6 cells transduced with CMV-eGFP adenovirus vector and their overlap with predicted highly conserved murine mouse targets of miR-132. (B) Ingenuity Pathway Analysis of significantly altered pathways in MIN6 cells overexpressing miR-132 and eGFP compared to MIN6 cells overexpressing eGFP alone. (C) Heat map of the 26 (red vertical bar: cluster of downregulated genes; blue vertical bar: cluster of upregulated genes) among the 345 differentially expressed genes included in the 8 regulated pathways indicated in (B) and related to cell proliferation and survival in MIN6 cells overexpressing miR-132 and eGFP relative to MIN6 cells overexpressing eGFP alone. The brightest shades of yellow and blue reflect the higher and lower expression levels of a given gene as indicated in the top horizontal bar. The results are from 3 independent microarray analyses. (D) Validation by RT-PCR of the expression levels of the top 10 most represented genes in the 8 signaling pathways shown in (B) and among the 26 regulated genes shown in (C). White bars: expression in MIN6 cells overexpressing eGFP alone; black bars: expression in MIN6 cells overexpressing miR-132 and eGFP. (E) Min6 cells were co-transfected with 1.5 ug of bicistronic vector psiCHECK-2 in which Pten-3′-UTR or Mapk1-3′-UTR were inserted downstream of the Renilla translational stop codon along with 100 nM of either control or miR-132 mimic oligonucleotide. Co-expressed firefly luciferase was used for the normalization of Renilla luciferase expression, and the luciferase activity of the control was set as 100% The data represent mean ± standard error from 3 separate experiments. *p < 0.05, **p < 0.01, **p < 0.001. (B) The significance was assessed using the Benjamini–Hochberg test.
Figure 4 Identification and validation of miR-132 target genes in MIN6 cells. (A) Venn diagram showing the number of down- and upregulated genes in MIN6 cells transduced with CMV-miR-132/eGFP adenovirus vector compared to MIN6 cells transduced with CMV-eGFP adenovirus vector and their overlap with predicted highly conserved murine mouse targets of miR-132. (B) Ingenuity Pathway Analysis of significantly altered pathways in MIN6 cells overexpressing miR-132 and eGFP compared to MIN6 cells overexpressing eGFP alone. (C) Heat map of the 26 (red vertical bar: cluster of downregulated genes; blue vertical bar: cluster of upregulated genes) among the 345 differentially expressed genes included in the 8 regulated pathways indicated in (B) and related to cell proliferation and survival in MIN6 cells overexpressing miR-132 and eGFP relative to MIN6 cells overexpressing eGFP alone. The brightest shades of yellow and blue reflect the higher and lower expression levels of a given gene as indicated in the top horizontal bar. The results are from 3 independent microarray analyses. (D) Validation by RT-PCR of the expression levels of the top 10 most represented genes in the 8 signaling pathways shown in (B) and among the 26 regulated genes shown in (C). White bars: expression in MIN6 cells overexpressing eGFP alone; black bars: expression in MIN6 cells overexpressing miR-132 and eGFP. (E) Min6 cells were co-transfected with 1.5 ug of bicistronic vector psiCHECK-2 in which Pten-3′-UTR or Mapk1-3′-UTR were inserted downstream of the Renilla translational stop codon along with 100 nM of either control or miR-132 mimic oligonucleotide. Co-expressed firefly luciferase was used for the normalization of Renilla luciferase expression, and the luciferase activity of the control was set as 100% The data represent mean ± standard error from 3 separate experiments. *p < 0.05, **p < 0.01, **p < 0.001. (B) The significance was assessed using the Benjamini–Hochberg test.CC BY-NC-ND · PubMed Central
Figure 5 Validation of gene profiling data in MIN6 cells overexpressing miR132. (A, C, and E) Representative immunoblots for the indicated proteins in cell extracts of MIN6 cells overexpressing miR-132 and eGFP or eGFP alone. (B, D, and F) Densitometric quantification of the indicated proteins as detected by immunblots in (A), (C), and (E), respectively. Data are from 6 independent experiments. *p < 0.05, **p < 0.01, **p < 0.001.
Figure 5 Validation of gene profiling data in MIN6 cells overexpressing miR132. (A, C, and E) Representative immunoblots for the indicated proteins in cell extracts of MIN6 cells overexpressing miR-132 and eGFP or eGFP alone. (B, D, and F) Densitometric quantification of the indicated proteins as detected by immunblots in (A), (C), and (E), respectively. Data are from 6 independent experiments. *p < 0.05, **p < 0.01, **p < 0.001.CC BY-NC-ND · PubMed Central
Figure 6 Impaired pancreatic beta cell regeneration in miR-132−/−mice. (A) Expression of blood glucose levels in wild-type (blue line) and miR-132−/− (red line) mice during an intraperitoneal glucose tolerance test conducted two days before surgery. (B) Expression of blood glucose levels in wild-type and miR-132−/− partially pancreatectomized or sham-operated mice during an intraperitoneal glucose tolerance test performed six days after surgery. Sham-operated wild-type mice: blue line; partially pancreatectomized wild-type mice: green line; sham-operated miR-132−/− mice: red line; partially pancreatectomized miR-132−/− mice: purple line. (C–F) Representative confocal images of paraffin pancreatic sections from wild-type sham-operated (C) or partially pancreatectomized mice (E) or from miR-132−/− sham-operated (D) or partially pancreatectomized (F) mice. Sections were immunolabeled for insulin (red) and BrdU (green), while nuclei were detected with DAPI (blue). (G) Percentage of BrdU+ and insulin+ cells. White bars: wild-type mice; black bars: miR-132−/− mice. Data are from 3 independent series with two mice in each group. Up to 50 islets were counted for each mouse for a total of 250–300 islets per group.
Figure 6 Impaired pancreatic beta cell regeneration in miR-132−/−mice. (A) Expression of blood glucose levels in wild-type (blue line) and miR-132−/− (red line) mice during an intraperitoneal glucose tolerance test conducted two days before surgery. (B) Expression of blood glucose levels in wild-type and miR-132−/− partially pancreatectomized or sham-operated mice during an intraperitoneal glucose tolerance test performed six days after surgery. Sham-operated wild-type mice: blue line; partially pancreatectomized wild-type mice: green line; sham-operated miR-132−/− mice: red line; partially pancreatectomized miR-132−/− mice: purple line. (C–F) Representative confocal images of paraffin pancreatic sections from wild-type sham-operated (C) or partially pancreatectomized mice (E) or from miR-132−/− sham-operated (D) or partially pancreatectomized (F) mice. Sections were immunolabeled for insulin (red) and BrdU (green), while nuclei were detected with DAPI (blue). (G) Percentage of BrdU+ and insulin+ cells. White bars: wild-type mice; black bars: miR-132−/− mice. Data are from 3 independent series with two mice in each group. Up to 50 islets were counted for each mouse for a total of 250–300 islets per group.CC BY-NC-ND · PubMed Central
Figure 7 Working model illustrating the miR-132 mediated control of cell survival and proliferation of pancreatic beta cells. Islet beta cell proliferation following partial pancreatectomy correlates with the upregulation of miR-132. MiR-132 reduces the expression of Pten, which in turn enhances Foxo3a phosphorylation. Phosphorylated Foxo3a is sequestered in the cytosol and its transcriptional activity of pro-apoptotic genes such as caspases is reduced. Repression of Pten activity also increases the levels of P-Akt and P-Creb and thus enhances cell proliferation. However, the involvement of Mapk/Erk signaling in miR-132-mediated beta cell proliferation is uncertain. Experimental data presented in this manuscript and literature-based knowledge are displayed as solid and dashed lines, respectively.
Figure 7 Working model illustrating the miR-132 mediated control of cell survival and proliferation of pancreatic beta cells. Islet beta cell proliferation following partial pancreatectomy correlates with the upregulation of miR-132. MiR-132 reduces the expression of Pten, which in turn enhances Foxo3a phosphorylation. Phosphorylated Foxo3a is sequestered in the cytosol and its transcriptional activity of pro-apoptotic genes such as caspases is reduced. Repression of Pten activity also increases the levels of P-Akt and P-Creb and thus enhances cell proliferation. However, the involvement of Mapk/Erk signaling in miR-132-mediated beta cell proliferation is uncertain. Experimental data presented in this manuscript and literature-based knowledge are displayed as solid and dashed lines, respectively.CC BY-NC-ND · PubMed Central

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Metadata

Authors
Mziaut, H., Henniger, G., Ganss, K., Hempel, S., Wolk, S., McChord, J., Chowdhury, K., Ravassard, P., Knoch, K.-P., Krautz, C., Weitz, J., Grützmann, R., Pilarsky, C., Solimena, M., & Kersting, S.
Venue
Molecular Metabolism
Publisher
Elsevier BV
Published
2020-01
Volume
31
Pages
150-162
ISSN
2212-8778
DOI
10.1016/j.molmet.2019.11.012
PMC
PMC6928290
Cited by
65
References
2
Language
en
Licence
Funders
  • Technische Universität Dresden
  • Bundesministerium für Bildung und Forschung

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Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: MiR-132 controls pancreatic beta cell proliferation and survival through Pten/Akt/Foxo3 signaling. https://app.cochat.ai/papers/10.1016/j.molmet.2019.11.012
The paper
Mziaut, H., Henniger, G., Ganss, K., Hempel, S., Wolk, S., McChord, J., Chowdhury, K., Ravassard, P., Knoch, K.-P., Krautz, C., Weitz, J., Grützmann, R., Pilarsky, C., Solimena, M., & Kersting, S. (2020). MiR-132 controls pancreatic beta cell proliferation and survival through Pten/Akt/Foxo3 signaling. Molecular Metabolism. https://doi.org/10.1016/j.molmet.2019.11.012