Gap junctions as modulators of adrenal cortical cell proliferation and steroidogenesis

Murray, Sandra A.; Nickel, Beth

doi:10.1016/j.mce.2008.09.027

Cited by 9 publications

(7 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Though not reviewed in this paper, it is worth noting that gap junctional communication is commonly dysregulated or even 'loosened' in tumor tissues [159], including endocrine gland neoplasms [24,147], complying with its involvement in the control of cell metabolism, cell growth and cell death. This strengthens the critical role of intercellular communication in the maintenance of vital physiological functions and body homeostasis [3].…”

Section: Discussionmentioning

confidence: 99%

“…[7,11,28] ? [7] processes, including differentiation, steroidogenesis and hormone responsiveness, migration and proliferation [22][23][24]. It is noteworthy that Cx43 exhibits a differential distribution pattern within the three zones of the adrenal cortex, which correlates with divergent proliferation rates and responsiveness to adrenocorticotropic hormone (ACTH).…”

Section: Connexin Intercellular Channelsmentioning

confidence: 99%

See 1 more Smart Citation

Roles of connexins and pannexins in (neuro)endocrine physiology

Hodson

Legros

Desarménien

et al. 2015

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

To ensure appropriate secretion in response to demand, (neuro)endocrine tissues liberate massive quantities of hormones, which act to coordinate and synchronize biological signals in distant secretory and nonsecretory cell populations. Intercellular communication plays a central role in this control. With regard to molecular identity, junctional cell-cell communication is supported by connexin-based gap junctions. In addition, connexin hemichannels, the structural precursors of gap junctions, as well as pannexin channels have recently emerged as possible modulators of the secretory process. This review focuses on the expression of connexins and pannexins in various (neuro)endocrine tissues, including the adrenal cortex and medulla, the anterior pituitary, the endocrine hypothalamus and the pineal, thyroid and parathyroid glands. Upon a physiological or pathological stimulus, junctional intercellular coupling can be acutely modulated or persistently remodeled, thus offering multiple regulatory possibilities. The functional roles of gap junction-mediated intercellular communication in endocrine physiology as well as the involvement of connexin/pannexin-related hemichannels are also discussed.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Connexin Intercellular Channelsmentioning

confidence: 99%

Roles of connexins and pannexins in (neuro)endocrine physiology

Hodson

Legros

Desarménien

et al. 2015

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

show abstract

“…Electrotonic coupling through the GJs ensures propagation of action potentials between cardiomyocytes (Rohr, 2004 ), synchronization of neuronal activity in various brain regions (Bennett and Zukin, 2004 ) and is an important component of retinal circuitry (Völgyi et al, 2013 ). GJs play an important role in non-excitable tissue as well, since intercellular cell signalling via GJs may orchestrate proliferation (Vance and Wiley, 1999 ; Murray et al, 2009 ) and apoptosis (Kameritsch et al, 2013 ; Akopian et al, 2014 ).…”

Section: Introductionmentioning

confidence: 99%

Modulation of Connexin-36 Gap Junction Channels by Intracellular pH and Magnesium Ions

et al. 2018

View full text Add to dashboard Cite

Connexin-36 (Cx36) protein forms gap junction (GJ) channels in pancreatic beta cells and is also the main Cx isoform forming electrical synapses in the adult mammalian brain. Cx36 GJs can be regulated by intracellular pH (pHi) and cytosolic magnesium ion concentration ([Mg2+]i), which can vary significantly under various physiological and pathological conditions. However, the combined effect and relationship of these two factors over Cx36-dependent coupling have not been previously studied in detail. Our experimental results in HeLa cells expressing Cx36 show that changes in both pHi and [Mg2+]i affect junctional conductance (gj) in an interdependent manner; in other words, intracellular acidification cause increase or decay in gj depending on whether [Mg2+]i is high or low, respectively, and intracellular alkalization cause reduction in gj independently of [Mg2+]i. Our experimental and modelling data support the hypothesis that Cx36 GJ channels contain two separate gating mechanisms, and both are differentially sensitive to changes in pHi and [Mg2+]i. Using recombinant Cx36 we found that two glutamate residues in the N-terminus could be partly responsible for the observed interrelated effect of pHi and [Mg2+]i. Mutation of glutamate at position 8 attenuated the stimulatory effect of intracellular acidification at high [Mg2+]i, while mutation at position 12 and double mutation at both positions reversed stimulatory effect to inhibition. Moreover, Cx36*E8Q lost the initial increase of gj at low [Mg2+]i and double mutation lost the sensitivity to high [Mg2+]i. These results suggest that E8 and E12 are involved in regulation of Cx36 GJ channels by Mg2+ and H+ ions.

show abstract

“…The first set of experiments, which demonstrated functional gap junction-mediated communication, were studies in which adrenal cells were placed into culture with ovarian granulosa cells. It is well documented that cells of the inner adrenal cortical zones possess specific receptors for ACTH and, when bound to its receptor, ACTH elicits a number of responses ( 62 , 63 ), including an activation of cAMP-dependent protein kinase A (PKA) ( 59 , 64 ), an increase in steroid synthesis ( 7 , 65 , 66 ), and a decrease in proliferation of cells in culture ( 2 , 8 , 67 ). In the adrenal/granulosa coculture populations, a cytochemical method was used to specifically localize free catalytic subunits (C) of PKA at subcellular, light microscopic levels of resolution ( 59 , 68 ).…”

Section: Role Of Gap Junctions In Adrenal Cortical Functionmentioning

confidence: 99%

Adrenocortical Gap Junctions and Their Functions

Bell

Murray

2016

Front. Endocrinol.

View full text Add to dashboard Cite

Adrenal cortical steroidogenesis and proliferation are thought to be modulated by gap junction-mediated direct cell–cell communication of regulatory molecules between cells. Such communication is regulated by the number of gap junction channels between contacting cells, the rate at which information flows between these channels, and the rate of channel turnover. Knowledge of the factors regulating gap junction-mediated communication and the turnover process are critical to an understanding of adrenal cortical cell functions, including development, hormonal response to adrenocorticotropin, and neoplastic dedifferentiation. Here, we review what is known about gap junctions in the adrenal gland, with particular attention to their role in adrenocortical cell steroidogenesis and proliferation. Information and insight gained from electrophysiological, molecular biological, and imaging (immunocytochemical, freeze fracture, transmission electron microscopic, and live cell) techniques will be provided.

show abstract

Gap junctions as modulators of adrenal cortical cell proliferation and steroidogenesis

Cited by 9 publications

References 50 publications

Roles of connexins and pannexins in (neuro)endocrine physiology

Roles of connexins and pannexins in (neuro)endocrine physiology

Modulation of Connexin-36 Gap Junction Channels by Intracellular pH and Magnesium Ions

Adrenocortical Gap Junctions and Their Functions

Contact Info

Product

Resources

About