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 |
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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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Pancreatic stellate cells augment the glucose‐stimulated insulin secretion from Min6 cells, with no possible involvement of IL6‐induced PLC‐IP3 ‐dependent pathway.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.29329</identifier><identifier>PMID: 31452250</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>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</subject><ispartof>Journal of cellular biochemistry, 2020-01, Vol.121 (1), p.840-855</ispartof><rights>2019 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3889-328031a56d853dcfb011deef49cfe0e93f5b5edeea08c76550dc6d39ac01d5633</citedby><cites>FETCH-LOGICAL-c3889-328031a56d853dcfb011deef49cfe0e93f5b5edeea08c76550dc6d39ac01d5633</cites><orcidid>0000-0002-3785-0530</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcb.29329$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.29329$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31452250$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bynigeri, Ratnakar R.</creatorcontrib><creatorcontrib>Mitnala, Sasikala</creatorcontrib><creatorcontrib>Talukdar, Rupjyoti</creatorcontrib><creatorcontrib>Singh, Surya S.</creatorcontrib><creatorcontrib>Duvvuru, Nageshwar R.</creatorcontrib><title>Pancreatic stellate cell‐potentiated insulin secretion from Min6 cells is independent of interleukin 6‐mediated pathway</title><title>Journal of cellular biochemistry</title><addtitle>J Cell Biochem</addtitle><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.</description><subject>Animals</subject><subject>Beta cells</subject><subject>Cell culture</subject><subject>Cells, Cultured</subject><subject>Coculture Techniques</subject><subject>Gene expression</subject><subject>Glucose</subject><subject>Glucose - pharmacology</subject><subject>Inhibitors</subject><subject>Inserts</subject><subject>Insulin</subject><subject>Insulin secretion</subject><subject>Insulin Secretion - drug effects</subject><subject>insulin secretion and miR‐375</subject><subject>Insulin-Secreting Cells - cytology</subject><subject>Insulin-Secreting Cells - drug effects</subject><subject>Insulin-Secreting Cells - metabolism</subject><subject>Insulinoma - metabolism</subject><subject>Insulinoma - pathology</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - metabolism</subject><subject>Mice</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Min6 cells</subject><subject>miRNA</subject><subject>Neomycin</subject><subject>Pancreas</subject><subject>Pancreatic diseases</subject><subject>pancreatic stellate cells</subject><subject>Pancreatic Stellate Cells - cytology</subject><subject>Pancreatic Stellate Cells - drug effects</subject><subject>Pancreatic Stellate Cells - metabolism</subject><subject>Polymerase chain reaction</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Secretions</subject><subject>Stellate cells</subject><subject>Sweetening Agents - pharmacology</subject><subject>Xestospongin C</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc9u1DAQhy0EokvhwAugSFzgkHZsx1nnSFf8q4rgAGfLa0-El6wTbEfViksfgWfkSTptCgekSpZHHn3-NJofY885nHAAcbpz2xPRSdE9YCsO3bpu2qZ5yFawllALycURe5LzDgA6oh6zI8kbJYSCFfv1xUaX0JbgqlxwGGzBylH9c_V7GgvGEqjjqxDzPIRYZSS6hDFWfRr31acQ21s8V4FO9DghXbFUY0_PgmnA-Qf9a8m3R7_IJlu-X9rDU_aot0PGZ3f1mH179_br5kN98fn9x82bi9pJrbtaCg2SW9V6raR3_RY494h907keATvZq61C6ljQbt0qBd61XnbWAfeqlfKYvVq8Uxp_zpiL2Yd8M7SNOM7ZCKE5B620JvTlf-hunFOk6Qztca2EVsCJer1QLo05J-zNlMLepoPhYG4SMZSIuU2E2Bd3xnlLC_hH_o2AgNMFuAwDHu43mfPN2aK8Bs94mJs</recordid><startdate>202001</startdate><enddate>202001</enddate><creator>Bynigeri, Ratnakar R.</creator><creator>Mitnala, Sasikala</creator><creator>Talukdar, Rupjyoti</creator><creator>Singh, Surya S.</creator><creator>Duvvuru, Nageshwar R.</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-3785-0530</orcidid></search><sort><creationdate>202001</creationdate><title>Pancreatic stellate cell‐potentiated insulin secretion from Min6 cells is independent of interleukin 6‐mediated pathway</title><author>Bynigeri, Ratnakar R. ; 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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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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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