Altered gap junction activity in cardiovascular tissues of diabetes

T. Inoguchi, Hai Yan Yu, Minako Imamura, Maiko Kakimoto, Tatsuya Kuroki, Toru Maruyama, Hajime Nawata

    Research output: Contribution to journalReview articlepeer-review

    51 Citations (Scopus)


    Hyperglycemia appears to be an important etiologic factor in the development of micro- and macrovascular complications in diabetic patients. However, its detailed molecular mechanism remains unclear. Among various possible mechanisms, it is widely accepted that high glucose level and a diabetic state induce protein kinase C (PKC) activation in vascular cells in cultured and vascular tissues of diabetic animals. Gap junctions are clusters of membrane channels that permit the intercellular exchange of ions and second messengers between adjacent cells. Gap junctional intercellular communication (GJIC) plays an important role in cardiovascular tissue homeostasis. Here we report that GJIC in cultured vascular cells such as endothelial cells and smooth muscle cells is inhibited by high glucose level. Furthermore, we show that it is mediated by PKC-dependent excessive phosphorylation of connexin-43 which is the main functional component of gap junction in vascular cells. In addition, we also show that in diabetic rats, PKC-dependent excessive phosphorylation of connexin-43 induces the impairment of ventricular conduction in the heart. These results suggest that PKC-dependent impairment of GJIC may lead to various disorders of cardiovascular homeostasis and contribute to cardiovascular dysfunctions associated with diabetes.

    Original languageEnglish
    Pages (from-to)86-91
    Number of pages6
    JournalMedical Electron Microscopy
    Issue number2
    Publication statusPublished - 2001

    All Science Journal Classification (ASJC) codes

    • Anatomy


    Dive into the research topics of 'Altered gap junction activity in cardiovascular tissues of diabetes'. Together they form a unique fingerprint.

    Cite this