Pancreatic stellate cell‐potentiated insulin secretion from Min6 cells is independent of interleukin 6‐mediated pathway

Pancreatic stellate cells (PSCs) secrete various factors, which can influence the β‐cell function. The identification of stellate cell infiltration into the islets in pancreatic diseases suggests possible existence of cross‐talk between these cells. To elucidate the influence of PSCs on β‐cell funct...

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Veröffentlicht in:Journal of cellular biochemistry 2020-01, Vol.121 (1), p.840-855
Hauptverfasser: Bynigeri, Ratnakar R., Mitnala, Sasikala, Talukdar, Rupjyoti, Singh, Surya S., Duvvuru, Nageshwar R.
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container_title Journal of cellular biochemistry
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creator Bynigeri, Ratnakar R.
Mitnala, Sasikala
Talukdar, Rupjyoti
Singh, Surya S.
Duvvuru, Nageshwar R.
description Pancreatic stellate cells (PSCs) secrete various factors, which can influence the β‐cell function. The identification of stellate cell infiltration into the islets in pancreatic diseases suggests possible existence of cross‐talk between these cells. To elucidate the influence of PSCs on β‐cell function, mouse PSCs were cocultured with Min6 cells using the Transwell inserts. Glucose‐stimulated insulin secretion from Min6 cells in response to PSCs was quantified by enzyme‐linked immunosorbent assay and insulin gene expression was measured by quantitative polymerase chain reaction. Upon cytometric identification of IL6 in PSC culture supernatants, Min6 cells were cultured with IL6 to assess its influence on the insulin secretion and gene expression. PLC‐IP3 pathway inhibitors were added in the cocultures, to determine the influence of PSC‐secreted IL6 on Glucose‐stimulated insulin secretion from Min6 cells. Increased insulin secretion with a concomitant decrease in total insulin content was noticed in PSC‐cocultured Min6 cells. Although increased GSIS was noted from IL6‐treated Min6 cells, no change in the total insulin content was noted. Coculture of Min6 cells with PSCs or their exposure to IL6 did not alter either the expression of β‐cell‐specific genes or that of miRNA‐375. PSC‐cocultured Min6 cells, in the presence of PLC‐IP3 pathway inhibitors (U73122, Neomycin, and Xestospongin C), did not revoke the observed increase in GSIS. In conclusion, the obtained results indicate that augmented insulin secretion from Min6 cells in response to PSC secretions is independent of IL6‐mediated PLC‐IP3 pathway. Pancreatic stellate cells augment the glucose‐stimulated insulin secretion from Min6 cells, with no possible involvement of IL6‐induced PLC‐IP3 ‐dependent pathway.
doi_str_mv 10.1002/jcb.29329
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The identification of stellate cell infiltration into the islets in pancreatic diseases suggests possible existence of cross‐talk between these cells. To elucidate the influence of PSCs on β‐cell function, mouse PSCs were cocultured with Min6 cells using the Transwell inserts. Glucose‐stimulated insulin secretion from Min6 cells in response to PSCs was quantified by enzyme‐linked immunosorbent assay and insulin gene expression was measured by quantitative polymerase chain reaction. Upon cytometric identification of IL6 in PSC culture supernatants, Min6 cells were cultured with IL6 to assess its influence on the insulin secretion and gene expression. PLC‐IP3 pathway inhibitors were added in the cocultures, to determine the influence of PSC‐secreted IL6 on Glucose‐stimulated insulin secretion from Min6 cells. Increased insulin secretion with a concomitant decrease in total insulin content was noticed in PSC‐cocultured Min6 cells. Although increased GSIS was noted from IL6‐treated Min6 cells, no change in the total insulin content was noted. Coculture of Min6 cells with PSCs or their exposure to IL6 did not alter either the expression of β‐cell‐specific genes or that of miRNA‐375. PSC‐cocultured Min6 cells, in the presence of PLC‐IP3 pathway inhibitors (U73122, Neomycin, and Xestospongin C), did not revoke the observed increase in GSIS. In conclusion, the obtained results indicate that augmented insulin secretion from Min6 cells in response to PSC secretions is independent of IL6‐mediated PLC‐IP3 pathway. 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The identification of stellate cell infiltration into the islets in pancreatic diseases suggests possible existence of cross‐talk between these cells. To elucidate the influence of PSCs on β‐cell function, mouse PSCs were cocultured with Min6 cells using the Transwell inserts. Glucose‐stimulated insulin secretion from Min6 cells in response to PSCs was quantified by enzyme‐linked immunosorbent assay and insulin gene expression was measured by quantitative polymerase chain reaction. Upon cytometric identification of IL6 in PSC culture supernatants, Min6 cells were cultured with IL6 to assess its influence on the insulin secretion and gene expression. PLC‐IP3 pathway inhibitors were added in the cocultures, to determine the influence of PSC‐secreted IL6 on Glucose‐stimulated insulin secretion from Min6 cells. Increased insulin secretion with a concomitant decrease in total insulin content was noticed in PSC‐cocultured Min6 cells. Although increased GSIS was noted from IL6‐treated Min6 cells, no change in the total insulin content was noted. Coculture of Min6 cells with PSCs or their exposure to IL6 did not alter either the expression of β‐cell‐specific genes or that of miRNA‐375. PSC‐cocultured Min6 cells, in the presence of PLC‐IP3 pathway inhibitors (U73122, Neomycin, and Xestospongin C), did not revoke the observed increase in GSIS. In conclusion, the obtained results indicate that augmented insulin secretion from Min6 cells in response to PSC secretions is independent of IL6‐mediated PLC‐IP3 pathway. 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The identification of stellate cell infiltration into the islets in pancreatic diseases suggests possible existence of cross‐talk between these cells. To elucidate the influence of PSCs on β‐cell function, mouse PSCs were cocultured with Min6 cells using the Transwell inserts. Glucose‐stimulated insulin secretion from Min6 cells in response to PSCs was quantified by enzyme‐linked immunosorbent assay and insulin gene expression was measured by quantitative polymerase chain reaction. Upon cytometric identification of IL6 in PSC culture supernatants, Min6 cells were cultured with IL6 to assess its influence on the insulin secretion and gene expression. PLC‐IP3 pathway inhibitors were added in the cocultures, to determine the influence of PSC‐secreted IL6 on Glucose‐stimulated insulin secretion from Min6 cells. Increased insulin secretion with a concomitant decrease in total insulin content was noticed in PSC‐cocultured Min6 cells. Although increased GSIS was noted from IL6‐treated Min6 cells, no change in the total insulin content was noted. Coculture of Min6 cells with PSCs or their exposure to IL6 did not alter either the expression of β‐cell‐specific genes or that of miRNA‐375. PSC‐cocultured Min6 cells, in the presence of PLC‐IP3 pathway inhibitors (U73122, Neomycin, and Xestospongin C), did not revoke the observed increase in GSIS. In conclusion, the obtained results indicate that augmented insulin secretion from Min6 cells in response to PSC secretions is independent of IL6‐mediated PLC‐IP3 pathway. Pancreatic stellate cells augment the glucose‐stimulated insulin secretion from Min6 cells, with no possible involvement of IL6‐induced PLC‐IP3 ‐dependent pathway.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>31452250</pmid><doi>10.1002/jcb.29329</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0002-3785-0530</orcidid><oa>free_for_read</oa></addata></record>
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source MEDLINE; Wiley Online Library Journals Frontfile Complete
subjects Animals
Beta cells
Cell culture
Cells, Cultured
Coculture Techniques
Gene expression
Glucose
Glucose - pharmacology
Inhibitors
Inserts
Insulin
Insulin secretion
Insulin Secretion - drug effects
insulin secretion and miR‐375
Insulin-Secreting Cells - cytology
Insulin-Secreting Cells - drug effects
Insulin-Secreting Cells - metabolism
Insulinoma - metabolism
Insulinoma - pathology
Interleukin 6
Interleukin-6 - metabolism
Mice
MicroRNAs - genetics
MicroRNAs - metabolism
Min6 cells
miRNA
Neomycin
Pancreas
Pancreatic diseases
pancreatic stellate cells
Pancreatic Stellate Cells - cytology
Pancreatic Stellate Cells - drug effects
Pancreatic Stellate Cells - metabolism
Polymerase chain reaction
Ribonucleic acid
RNA
Secretions
Stellate cells
Sweetening Agents - pharmacology
Xestospongin C
title Pancreatic stellate cell‐potentiated insulin secretion from Min6 cells is independent of interleukin 6‐mediated pathway
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