| Literature DB >> 29855712 |
Hongliang Li1, Sung Eun Shin1, Mi Seon Seo1, Jin Ryeol An1, Kwon-Soo Ha2, Eun-Taek Han3, Seok-Ho Hong4, Jeeyoung Kim4, Mi-Jin Yim5, Jeong Min Lee5, Tae Gyu An6, Jihan Jeon6, Se Jin Lee6, Sung Hun Na7, Won Sun Park8.
Abstract
We investigated the alterations of ATP-sensitive K+ (KATP) channels in human umbilical arterial smooth muscle cells during gestational diabetes mellitus (GDM). The amplitude of the KATP current induced by application of the KATP channel opener pinacidil (10 μM) was reduced in the GDM group than in the control group. Pinacidil-induced vasorelaxation was also predominant in the normal group compared with the GDM group. Reverse transcription polymerase chain reaction and Western blot analysis suggested that the expression of KATP channel subunits such as Kir6.1, Kir6.2, and SUR2B were decreased in the GDM group relative to the normal group. The application of forskolin and adenosine, which activates protein kinase A (PKA) and thereby KATP channels, elicited KATP current in both the normal and GDM groups. However, the current amplitudes were not different between the normal and GDM groups. In addition, the expression levels of PKA subunits were not altered between the two groups. These results suggest that the reduction of KATP current and KATP channel-induced vasorelaxation are due to the decreased expression of KATP channels, not to the impairment of KATP-related signaling pathways.Entities:
Keywords: ATP-sensitive K+ channels; Gestational diabetes mellitus; Protein kinase A; Umbilical artery
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Year: 2018 PMID: 29855712 DOI: 10.1007/s00424-018-2154-8
Source DB: PubMed Journal: Pflugers Arch ISSN: 0031-6768 Impact factor: 3.657