کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8476353 | 1550806 | 2018 | 28 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
High glucose up-regulates Semaphorin 3A expression via the mTOR signaling pathway in keratinocytes: A potential mechanism and therapeutic target for diabetic small fiber neuropathy
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کلمات کلیدی
4E-BP1eukaryotic initiation factor 4E-binding protein 1p70 S6KSNCVIENFDFPGDRGSema3AWPTNSSDPNSTZSFNCPTmTORp70 ribosomal protein S6 kinase - P70 پروتئین ریبوزومی S6 کینازqst - QSTstreptozotocin - استرپتوزوتوسینIntraepidermal nerve fibers - الیاف عصبی درون اپیدرمالOct - اکتبرIntraepidermal nerve fiber density - تراکم فیبر داخل عضلانیoptimal cutting temperature compound - ترکیب دما برش مطلوبQuantitative Sensory Testing - تست حساسیت کمیAtopic dermatitis - درماتیت آتوپیکSemaphorin 3A - سمافورین 3ASNAP - ضربه محکم و ناگهانیFasting plasma glucose - قند خون ناشتاSmall fiber neuropathy - نوروپاتی فیبر کوچکdiabetic peripheral neuropathy - نوروپاتی محیطی دیابتیmammalian target of rapamycin - هدف پستانداران رپامایسینKeratinocyte - کراتینوسیتhigh glucose - گلوکز بالا یا قند بالا
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Small fiber neuropathy (SFN) is a common complication in diabetes, and is characterized by decreased intraepidermal nerve fiber density (IENFD). Semaphorin 3A (Sema3A), which is produced by keratinocytes, has a chemorepulsive effect on intraepidermal nerve fibers. mTOR signaling can mediate local protein synthesis that is critical for growth of axons and dendrites. Therefore, this study aimed to investigate whether Sema3A is up-regulated in diabetic keratinocytes via the mTOR-mediated p70 S6K and 4E-BP1 signaling pathways, and furthermore whether it is involved in the pathogenesis of diabetic SFN. IENFD, expression of Sema3A, and mTOR signaling, were evaluated in the skin of diabetic patients with SFN as well as control subjects. Sema3A and mTOR signaling were also assessed in HaCaT cells which had been treated with high glucose (HG) or recombinant Sema3A (rSema3A) in the presence or absence of rapamycin. Small fiber dysfunction was evaluated by examining IENFD and using behavioral tests in control and streptozotocin-induced diabetic rats treated with or without rapamycin. We found that higher Sema3A expression and over-activation of mTOR signaling, was accompanied by reduced IENFD in the skin of diabetic patients compared with control subjects. The expression of Sema3A, and mTOR signaling were up-regulated in HaCaT cells incubated with HG or rSema3A, and this could be attenuated by rapamycin. Hyperalgesia, reduced IENFD, and up-regulated Sema3A and mTOR signaling were also detected in diabetic rats. These effects were ameliorated by rapamycin treatment. Our data indicate that HG up-regulates Sema3A expression by activating mTOR signaling in diabetic keratinocytes. This pathway may therefore play a critical role in diabetic SFN.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Endocrinology - Volume 472, 5 September 2018, Pages 107-116
Journal: Molecular and Cellular Endocrinology - Volume 472, 5 September 2018, Pages 107-116
نویسندگان
Liang-yan Wu, Mei Li, Min-Li Qu, Xin Li, Lin-Hua Pi, Zi Chen, Shan-Lei Zhou, Xiao-Qing Yi, Xia-Jie Shi, Jing Wu, Shan Wang,