Role of Heterocellular Gap Junctional Communication in Endothelium-Dependent Smooth Muscle Hyperpolarization: Inhibition by a Connexin-Mimetic Peptide

1999 ◽  
Vol 254 (1) ◽  
pp. 27-31 ◽  
Author(s):  
K Dora
Keyword(s):  
Smooth Muscle ◽  
Mimetic Peptide ◽  
Gap Junctional Communication ◽  
Junctional Communication ◽  
Gap Junctional

Role of gap junctional communication in restitution of rat gastric mucosa

1998 ◽  
Vol 114 ◽  
pp. A302-A303
Author(s):  
N. Takahashi ◽  
T. Joh ◽  
K. Seno ◽  
K. Watanabe ◽  
K. Tsuchida ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Gap Junctional Communication ◽  
Junctional Communication ◽  
Rat Gastric Mucosa ◽  
Gap Junctional

scholarly journals The connexin43 mimetic peptide Gap19 inhibits hemichannels without altering gap junctional communication in astrocytes

2014 ◽  
Vol 8 ◽  
Author(s):  
Verónica Abudara ◽  
John Bechberger ◽  
Moises Freitas-Andrade ◽  
Marijke De Bock ◽  
Nan Wang ◽  
...  
Keyword(s):  
Mimetic Peptide ◽  
Gap Junctional Communication ◽  
Junctional Communication ◽  
Gap Junctional

scholarly journals Involvement of connexin 43 phosphorylation and gap junctional communication between smooth muscle cells in vasopressin-induced ROCK-dependent vasoconstriction after hemorrhagic shock

2017 ◽  
Vol 313 (4) ◽  
pp. C362-C370 ◽  
Author(s):  
Guangming Yang ◽  
Xiaoyong Peng ◽  
Yue Wu ◽  
Tao Li ◽  
Liangming Liu
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Gap Junctions ◽  
Hemorrhagic Shock ◽  
Connexin 43 ◽  
Muscle Cells ◽  
Gap Junctional Communication ◽  
Contractile Effect ◽  
Junctional Communication ◽  
Gap Junctional

We examined the roles played by gap junctions (GJs) and the GJ channel protein connexin 43 (Cx43) in arginine vasopressin (AVP)-induced vasoconstriction after hemorrhagic shock and their relationship to Rho kinase (ROCK) and protein kinase C (PKC). The results showed that AVP induced an endothelium-independent contraction in rat superior mesenteric arteries (SMAs). Blocking the GJs significantly decreased the contractile response of SMAs and vascular smooth muscle cells (VSMCs) to AVP after shock and hypoxia. The selective Cx43-mimetic peptide inhibited the vascular contractile effect of AVP after shock and hypoxia. AVP restored hypoxia-induced decrease of Cx43 phosphorylation at Ser262 and gap junctional communication in VSMCs. Activation of RhoA with U-46619 increased the contractile effect of AVP. This effect was antagonized by the ROCK inhibitor Y27632 and the Cx43-mimetic peptide. In contrast, neither an agonist nor an inhibitor of PKC had significant effects on AVP-induced contraction after hemorrhagic shock. In addition, silencing of Cx43 with siRNA blocked the AVP-induced increase of ROCK activity in hypoxic VSMCs. In conclusion, AVP-mediated vascular contractile effects are endothelium and myoendothelial gap junction independent. Gap junctions between VSMCs, gap junctional communication, and Cx43 phosphorylation at Ser262 play important roles in the vascular effects of AVP. RhoA/ROCK, but not PKC, is involved in this process.

scholarly journals Intercellular Conduction Optimizes Arterial Network Function and Conserves Blood Flow Homeostasis during Cerebrovascular Challenges

2019 ◽  
Author(s):  
Anil Zechariah ◽  
Cam Ha T. Tran ◽  
Bjorn O. Hald ◽  
Shaun L. Sandow ◽  
Maria Sancho ◽  
...  
Keyword(s):  
Blood Flow ◽  
Tissue Injury ◽  
Vascular Cells ◽  
Arterial Tree ◽  
Gap Junctional Communication ◽  
Arterial Network ◽  
Junctional Communication ◽  
Electrical Signalling ◽  
Gap Junctional

AbstractCerebral arterial networks match blood flow delivery with neural activity. Neurovascular response begins with a stimulus and a focal change in vessel diameter, which by themselves is inconsequential to blood flow magnitude, until they spread and alter the contractile status of neighboring arterial segments. We sought to define the mechanisms underlying integrated vascular behavior and considered the role of intercellular electrical signalling in this phenomenon. Electron microscopic and histochemical analysis revealed the structural coupling of cerebrovascular cells and the expression of gap junctional subunits at the cell interfaces, enabling intercellular signaling among vascular cells. Indeed, robust vasomotor conduction was detected in human and mice cerebral arteries after focal vessel stimulation; a response attributed to endothelial gap junctional communication, as its genetic alteration attenuated this behavior. Conducted responses was observed to ascend from the penetrating arterioles, influencing the contractile status of cortical surface vessels, in a simulated model of cerebral arterial network. Ascending responses recognised in vivo after whisker stimulation, were significantly attenuated in mice with altered endothelial gap junctional signalling confirming that gap junctional communication drives integrated vessel responses. The diminishment in vascular communication also impaired the critical ability of the cerebral vasculature to maintain blood flow homeostasis and hence tissue viability, after stroke. Our findings establish the integral role of intercellular electrical signalling in transcribing focal stimuli into coordinated changes in cerebrovascular contractile activity and expose, a hitherto unknown mechanism for flow regulation after stroke.SignificanceNeurovascular responses are viewed as a one step process whereby stimuli derived from neural cells focally diffuse to a neighboring vessel, altering its contractile state. While focal changes in tone can subtly tune flow distribution, they can’t substantively change “perfusion magnitude” as vascular resistance is broadly distributed along the cerebral arterial tree. We report that nature overcomes this biophysical constraint by conducting electrical signals among coupled vascular cells, along vessels, and across branch points. Our quantitative exploration of intercellular conduction illustrates how network coordination optimizes blood flow delivery in support of brain function. Diminishing the ability of vascular cells to electrically communicate, mitigates the brain’s ability to regulate perfusion during functional hyperemia and after stroke, the latter advancing tissue injury.

The role of gap junctions in patterning of the chick limb bud

Development ◽  
1990 ◽  
Vol 108 (4) ◽  
pp. 623-634 ◽  
Author(s):  
F. Allen ◽  
C. Tickle ◽  
A. Warner
Keyword(s):  
Gap Junctions ◽  
Lucifer Yellow ◽  
Limb Bud ◽  
Limb Patterning ◽  
Posterior Limb ◽  
Gap Junctional Communication ◽  
Junctional Communication ◽  
Mesenchyme Cells ◽  
Gap Junctional

The role of gap junctional communication during patterning of the chick limb has been investigated. Affinity-purified antibodies raised against rat liver gap junctional proteins were used to block communication between limb mesenchyme cells. Co-injection of the antibodies and Lucifer yellow into mesenchyme cultures demonstrated that communication was inhibited almost immediately. When antibodies were loaded into mesenchyme tissue by DMSO permeabilization, [3H]nucleotide transfer was prevented for at least 16 h. Polarizing region tissue from the posterior limb bud margin causes digit duplications when grafted to the anterior margin. Quail polarizing region cells were loaded with gap junction antibody and grafted into chick wing buds. The antibody had no effect on growth or survival of the grafted cells. As very few polarizing region cells are required to initiate duplications, the number of polarizing region cells in the grafts was reduced by diluting 1:9 with anterior mesenchyme tissue. When either polarizing region or anterior mesenchyme tissue in the graft was loaded separately with antibody, there was little effect on respecification of the digit pattern. However, loading both tissues in the graft caused a significant decrease in duplications. This indicates that a major role of gap junctions in limb patterning may be to enable polarizing region cells to communicate directly with adjacent anterior mesenchyme. A role for gap junctional communication between anterior mesenchyme cells cannot be excluded. The results are discussed in relation to the role of retinoic acid as a putative morphogen.

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