LncRNA MALAT1 induces the dysfunction of β cells via reducing the histone acetylation of the PDX-1 promoter in type 1 diabetes
Type 1 diabetes (T1DM) severely threatens human health, and the dysfunction of insulin-secreting β cells in islets is related to the reduced PDX-1 expression. It has been reported that long non-coding RNA MALAT1 regulates β cell function, while the potential mechanism is unclear. Islets were isolate...
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| Published in | Experimental and molecular pathology Vol. 114; p. 104432 |
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| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier Inc
01.06.2020
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| Online Access | Get full text |
| ISSN | 0014-4800 1096-0945 1096-0945 |
| DOI | 10.1016/j.yexmp.2020.104432 |
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| Abstract | Type 1 diabetes (T1DM) severely threatens human health, and the dysfunction of insulin-secreting β cells in islets is related to the reduced PDX-1 expression. It has been reported that long non-coding RNA MALAT1 regulates β cell function, while the potential mechanism is unclear.
Islets were isolated from non-obese diabetic (NOD) mice and wild type (WT) mice. Mouse islets and β cell line (Min6) were stimulated by IL-1β. The expression of MALAT1 was determined using real-time PCR, while the PDX-1 protein expression was determined using western blotting. ChIP-qPCR was carried out to determine the histone acetylation of the PDX-1 promoter.
In NOD islets and IL-1β-stimulated Min6 cells, the expression of MALAT1 was increased, while the mRNA and protein levels of PDX-1 were decreased at an age/time-dependent manner. Overexpressing MALAT1 suppressed the H3 histone acetylation of the PDX-1 promoter, inhibiting both mRNA and protein expressions of PDX-1. Knocking down MALAT1 restored the decrease of the histone acetylation of the PDX-1 promoter, as well as the PDX-1 expression, which was reduced by IL-1β stimulation. Under high glucose stimulation, the overexpression of PDX-1 alone restored the insulin secretion which was inhibited by the simultaneous overexpression of MALAT1 and PDX-1. Under high glucose and IL-1β stimulation, the simultaneous knockdown of MALAT1 and PDX-1 reduced the enhancement of the insulin secretion which was raised by knocking down MALAT1 alone.
MALAT1 induces the dysfunction of β cells via reducing the H3 histone acetylation of the PDX-1 promoter and subsequently inhibiting the expression of PDX-1, thus suppressing the insulin secretion. |
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| AbstractList | Type 1 diabetes (T1DM) severely threatens human health, and the dysfunction of insulin-secreting β cells in islets is related to the reduced PDX-1 expression. It has been reported that long non-coding RNA MALAT1 regulates β cell function, while the potential mechanism is unclear.
Islets were isolated from non-obese diabetic (NOD) mice and wild type (WT) mice. Mouse islets and β cell line (Min6) were stimulated by IL-1β. The expression of MALAT1 was determined using real-time PCR, while the PDX-1 protein expression was determined using western blotting. ChIP-qPCR was carried out to determine the histone acetylation of the PDX-1 promoter.
In NOD islets and IL-1β-stimulated Min6 cells, the expression of MALAT1 was increased, while the mRNA and protein levels of PDX-1 were decreased at an age/time-dependent manner. Overexpressing MALAT1 suppressed the H3 histone acetylation of the PDX-1 promoter, inhibiting both mRNA and protein expressions of PDX-1. Knocking down MALAT1 restored the decrease of the histone acetylation of the PDX-1 promoter, as well as the PDX-1 expression, which was reduced by IL-1β stimulation. Under high glucose stimulation, the overexpression of PDX-1 alone restored the insulin secretion which was inhibited by the simultaneous overexpression of MALAT1 and PDX-1. Under high glucose and IL-1β stimulation, the simultaneous knockdown of MALAT1 and PDX-1 reduced the enhancement of the insulin secretion which was raised by knocking down MALAT1 alone.
MALAT1 induces the dysfunction of β cells via reducing the H3 histone acetylation of the PDX-1 promoter and subsequently inhibiting the expression of PDX-1, thus suppressing the insulin secretion. Type 1 diabetes (T1DM) severely threatens human health, and the dysfunction of insulin-secreting β cells in islets is related to the reduced PDX-1 expression. It has been reported that long non-coding RNA MALAT1 regulates β cell function, while the potential mechanism is unclear.BACKGROUNDType 1 diabetes (T1DM) severely threatens human health, and the dysfunction of insulin-secreting β cells in islets is related to the reduced PDX-1 expression. It has been reported that long non-coding RNA MALAT1 regulates β cell function, while the potential mechanism is unclear.Islets were isolated from non-obese diabetic (NOD) mice and wild type (WT) mice. Mouse islets and β cell line (Min6) were stimulated by IL-1β. The expression of MALAT1 was determined using real-time PCR, while the PDX-1 protein expression was determined using western blotting. ChIP-qPCR was carried out to determine the histone acetylation of the PDX-1 promoter.METHODSIslets were isolated from non-obese diabetic (NOD) mice and wild type (WT) mice. Mouse islets and β cell line (Min6) were stimulated by IL-1β. The expression of MALAT1 was determined using real-time PCR, while the PDX-1 protein expression was determined using western blotting. ChIP-qPCR was carried out to determine the histone acetylation of the PDX-1 promoter.In NOD islets and IL-1β-stimulated Min6 cells, the expression of MALAT1 was increased, while the mRNA and protein levels of PDX-1 were decreased at an age/time-dependent manner. Overexpressing MALAT1 suppressed the H3 histone acetylation of the PDX-1 promoter, inhibiting both mRNA and protein expressions of PDX-1. Knocking down MALAT1 restored the decrease of the histone acetylation of the PDX-1 promoter, as well as the PDX-1 expression, which was reduced by IL-1β stimulation. Under high glucose stimulation, the overexpression of PDX-1 alone restored the insulin secretion which was inhibited by the simultaneous overexpression of MALAT1 and PDX-1. Under high glucose and IL-1β stimulation, the simultaneous knockdown of MALAT1 and PDX-1 reduced the enhancement of the insulin secretion which was raised by knocking down MALAT1 alone.RESULTSIn NOD islets and IL-1β-stimulated Min6 cells, the expression of MALAT1 was increased, while the mRNA and protein levels of PDX-1 were decreased at an age/time-dependent manner. Overexpressing MALAT1 suppressed the H3 histone acetylation of the PDX-1 promoter, inhibiting both mRNA and protein expressions of PDX-1. Knocking down MALAT1 restored the decrease of the histone acetylation of the PDX-1 promoter, as well as the PDX-1 expression, which was reduced by IL-1β stimulation. Under high glucose stimulation, the overexpression of PDX-1 alone restored the insulin secretion which was inhibited by the simultaneous overexpression of MALAT1 and PDX-1. Under high glucose and IL-1β stimulation, the simultaneous knockdown of MALAT1 and PDX-1 reduced the enhancement of the insulin secretion which was raised by knocking down MALAT1 alone.MALAT1 induces the dysfunction of β cells via reducing the H3 histone acetylation of the PDX-1 promoter and subsequently inhibiting the expression of PDX-1, thus suppressing the insulin secretion.CONCLUSIONMALAT1 induces the dysfunction of β cells via reducing the H3 histone acetylation of the PDX-1 promoter and subsequently inhibiting the expression of PDX-1, thus suppressing the insulin secretion. |
| ArticleNumber | 104432 |
| Author | Ma, Hongfang Du, Yaping Hou, Lin Wang, Fujun Ding, Haixia Xing, Na Shi, Xuelian |
| Author_xml | – sequence: 1 givenname: Haixia surname: Ding fullname: Ding, Haixia organization: Department of Endocrinology, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050000, China – sequence: 2 givenname: Fujun surname: Wang fullname: Wang, Fujun email: wangfujun139@126.com organization: Department of Endocrinology, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050000, China – sequence: 3 givenname: Xuelian surname: Shi fullname: Shi, Xuelian organization: Department of Pain rehabilitation, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China – sequence: 4 givenname: Hongfang surname: Ma fullname: Ma, Hongfang organization: Department of Endocrinology, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050000, China – sequence: 5 givenname: Yaping surname: Du fullname: Du, Yaping organization: Department of Endocrinology, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050000, China – sequence: 6 givenname: Lin surname: Hou fullname: Hou, Lin organization: Department of Endocrinology, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050000, China – sequence: 7 givenname: Na surname: Xing fullname: Xing, Na organization: Department of Endocrinology, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050000, China |
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| Title | LncRNA MALAT1 induces the dysfunction of β cells via reducing the histone acetylation of the PDX-1 promoter in type 1 diabetes |
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