Archives

  • 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • N Cadherin facilitated gap junction formation between embryo

    2022-05-19

    N-Cadherin facilitated gap junction formation between embryonic lens Cinacalcet HCl by stabilizing membrane appositions (Frenzel and Johnson, 1996). Cx43 has been found to be delivered to N-Cadherin-positive membrane HeLa cells (Shaw et al., 2007), and N-Cadherin determine the localization of Cx43 in cardiac myocytes (Matsuda et al., 2006). GC promoted the translocation of the GC-GR complex to the nucleus, resulting in the decrease of N-cadherin (Celojevic et al., 2012, Lecanda et al., 2000, Lyu et al., 2003). Therefore, downregulation of Cx43 in the membrane may result from decreased expression of N-Cadherin in hippocampal astrocytes in the present study. However, CORT increased the expression of N-Cadherin in prefrontal cortical astrocytes. Then, we considered the function of N-Cadherin. Previous studies have noted that cadherin-mediated cell-cell contact facilitates the assembly of connexins to gap junctions (Govindarajan et al., 2010). Therefore, we hypothesized that upregulation of N-Cadherin enhances the cell-cell contact, thereby promoting the formation of double membranes of annular gap junction vesicles in prefrontal cortical astrocytes. On the contrary, N-Cadherin has been found to promote a non clathrin-mediated endocytosis of Cx43 before its assembly into functional gap junctions (Govindarajan et al., 2010). Thus, whether N-Cadherin participates in the endocytosis of Cx43 in prefrontal cortical astrocytes, or plays different roles in prefrontal cortical and hippocampal astrocytes, requires further study. Moreover, ZO-1 has been found to regulate the stable localization of adherens junctions (Palatinus et al., 2011); thus, distinct alternations of ZO-1 in prefrontal cortical and hippocampal astrocytes may contribute to the different changes in N-Cadherin. CORT-induced different changes between prefrontal cortical astrocytes and hippocampal astrocytes may result from region-differences of prefrontal cortex and hippocampus. Prefrontal cortex and hippocampus showed different susceptibility to chronic social isolation stress. The prefrontal cortex was more sensitive to oxidative stress than the hippocampus following chronic isolation stress (Zlatkovic et al., 2014). CORT treatment (10 mg/kg, once daily for 21 days) of wild-type mice resulted in a decrease in 5-HT1A receptor function in prefrontal cortex, but not in hippocampus (Hensler et al., 2010). In monkeys exposed to adult social stress, GR expression but not MR was diminished in hippocampal CA1, whereas MR but not GR was diminished in cell layer III of ventrolateral prefrontal cortex (Patel et al., 2008). Thus, the different regulation of MR/GR in prefrontal cortex and hippocampus may result in the divergence of prefrontal cortex and hippocampus in response to stress. Moreover, nine putative 'types' of astrocytes were found in the murine CNS based on morphology and expression of astrocyte-enriched proteins. Astrocytes were diverse in different brain region and even in a given brain region (Ben Haim and Rowitch, 2017, Matyash and Kettenmann, 2010). Therefore, different astrocytes type in prefrontal cortex and hippocampus may result in the divergence in the CORT-induced changes between prefrontal cortex and hippocampus. In conclusion, CORT-induced alternations of the Cx43 life cycle in prefrontal cortical and hippocampal astrocytes are suggestive of a possible mechanism for the dysfunction of gap junctions under stress. Though the mechanism underlying CUS-induced dysfunction of gap junctions should be confirmed in vivo, the present study identified the biosynthesis, stability and degradation of Cx43 as potential targets for the regulation of gap junctions under stress, which may be benefit for depression therapy.
    Conflicts of interest
    Authors contribution