Hormonal regulation of intercellular communication: parathyroid hormone increases connexin 43 gene expression and gap-junctional communication in osteoblastic cells

1992 ◽  
Vol 6 (9) ◽  
pp. 1433-1440 ◽  
Author(s):  
P. C. Schiller
Keyword(s):  
Gene Expression ◽  
Parathyroid Hormone ◽  
Intercellular Communication ◽  
Hormonal Regulation ◽  
Connexin 43 ◽  
Osteoblastic Cells ◽  
Gap Junctional Communication ◽  
Junctional Communication ◽  
Gap Junctional

scholarly journals Hormonal Regulation of Connexin 43 Expression and Gap Junctional Communication in Human Osteoblastic Cells.

1994 ◽  
Vol 19 (3) ◽  
pp. 173-177 ◽  
Author(s):  
Hideki Chiba ◽  
Norimasa Sawada ◽  
Masahito Oyamada ◽  
Takashi Kojima ◽  
Kousuke Iba ◽  
...  
Keyword(s):  
Hormonal Regulation ◽  
Connexin 43 ◽  
Osteoblastic Cells ◽  
Gap Junctional Communication ◽  
Junctional Communication ◽  
Gap Junctional ◽  
Human Osteoblastic Cells

Gap junction-mediated transfer of left-right patterning signals in the early chick blastoderm is upstream of Shh asymmetry in the node

Development ◽  
1999 ◽  
Vol 126 (21) ◽  
pp. 4703-4714 ◽  
Author(s):  
M. Levin ◽  
M. Mercola
Keyword(s):  
Gene Expression ◽  
Gap Junction ◽  
Large Scale ◽  
Chick Blastoderm ◽  
Gap Junction Channels ◽  
Gap Junctional Communication ◽  
Junctional Communication ◽  
Left And Right ◽  
The Right ◽  
Gap Junctional

Invariant patterning of left-right asymmetry during embryogenesis depends upon a cascade of inductive and repressive interactions between asymmetrically expressed genes. Different cascades of asymmetric genes distinguish the left and right sides of the embryo and are maintained by a midline barrier. As such, the left and right sides of an embryo can be viewed as distinct and autonomous fields. Here we describe a series of experiments that indicate that the initiation of these programs requires communication between the two sides of the blastoderm. When deprived of either the left or the right lateral halves of the blastoderm, embryos are incapable of patterning normal left-right gene expression at Hensen's node. Not only are both flanks required, suggesting that there is no single signaling source for LR pattern, but the blastoderm must be intact. These results are consistent with our previously proposed model in which the orientation of LR asymmetry in the frog, Xenopus laevis, depends on large-scale partitioning of LR determinants through intercellular gap junction channels (M. Levin and M. Mercola (1998) Developmental Biology 203, 90–105). Here we evaluate whether gap junctional communication is required for the LR asymmetry in the chick, where it is possible to order early events relative to the well-characterized left and right hierarchies of gene expression. Treatment of cultured chick embryos with lindane, which diminishes gap junctional communication, frequently unbiased normal LR asymmetry of Shh and Nodal gene expression, causing the normally left-sided program to be recapitulated symmetrically on the right side of the embryo. A survey of early expression of connexin mRNAs revealed that Cx43 is present throughout the blastoderm at Hamburger-Hamilton stage 2–3, prior to known asymmetric gene expression. Application of antisense oligodeoxynucleotides or blocking antibody to cultured embryos also resulted in bilateral expression of Shh and Nodal transcripts. Importantly, the node and primitive streak at these stages lack Cx43 mRNA. This result, together with the requirement for an intact blastoderm, suggests that the path of communication through gap junction channels circumvents the node and streak. We propose that left-right information is transferred unidirectionally throughout the epiblast by gap junction channels in order to pattern left-sided Shh expression at Hensen's node.

Gap-junctional communication is required for the maturation process of osteoblastic cells in culture

Bone ◽  
2001 ◽  
Vol 28 (4) ◽  
pp. 362-369 ◽  
Author(s):  
P.C Schiller ◽  
G D’Ippolito ◽  
W Balkan ◽  
B.A Roos ◽  
G.A Howard
Keyword(s):  
Osteoblastic Cells ◽  
Maturation Process ◽  
Gap Junctional Communication ◽  
Cells In Culture ◽  
Junctional Communication ◽  
Gap Junctional

Inhibition of gap junctional communication by polyunsaturated fatty acids in WB cells: evidence that connexin 43 is not hyperphosphorylated

1995 ◽  
Vol 16 (7) ◽  
pp. 1505-1511 ◽  
Author(s):  
Charles S. T. Hii ◽  
Antonio Ferrante ◽  
Simon Schmidt ◽  
Deborah A. Rathjen ◽  
Brenton S. Robinson ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Connexin 43 ◽  
Gap Junctional Communication ◽  
Junctional Communication ◽  
Gap Junctional

scholarly journals Polyamines preserve connexin 43-mediated gap junctional communication during intracellular hypercalcemia and acidosis

Neuroreport ◽  
2017 ◽  
Vol 28 (4) ◽  
pp. 208-213 ◽  
Author(s):  
Lilia Y. Kucheryavykh ◽  
Jan Benedikt ◽  
Luis A. Cubano ◽  
Serguei N. Skatchkov ◽  
Feliksas F. Bukauskas ◽  
...  
Keyword(s):  
Connexin 43 ◽  
Gap Junctional Communication ◽  
Junctional Communication ◽  
Gap Junctional

Differentiation of human fetal osteoblastic cells and gap junctional intercellular communication

2000 ◽  
Vol 278 (2) ◽  
pp. C315-C322 ◽  
Author(s):  
Henry J. Donahue ◽  
Zhongyong Li ◽  
Zhiyi Zhou ◽  
Clare E. Yellowley
Keyword(s):  
Alkaline Phosphatase ◽  
Gap Junction ◽  
Phosphatase Activity ◽  
Alkaline Phosphatase Activity ◽  
Intercellular Communication ◽  
Connexin 43 ◽  
Osteoblastic Cells ◽  
Gap Junctional Intercellular Communication ◽  
Osteoblastic Cell Line ◽  
Gap Junctional

Gap junctional channels facilitate intercellular communication and in doing so may contribute to cellular differentiation. To test this hypothesis, we examined gap junction expression and function in a temperature-sensitive human fetal osteoblastic cell line (hFOB 1.19) that when cultured at 37°C proliferates rapidly but when cultured at 39.5°C proliferates slowly and displays increased alkaline phosphatase activity and osteocalcin synthesis. We found that hFOB 1.19 cells express abundant connexin 43 (Cx43) protein and mRNA. In contrast, Cx45 mRNA was expressed to a lesser degree, and Cx26 and Cx32 mRNA were not detected. Culturing hFOB 1.19 cells at 39.5°C, relative to 37°C, inhibited proliferation, increased Cx43 mRNA and protein expression, and increased gap junctional intercellular communication (GJIC). Blocking GJIC with 18α-glycyrrhetinic acid prevented the increase in alkaline phosphatase activity resulting from culture at 39.5°C but did not affect osteocalcin levels. These results suggest that gap junction function and expression parallel osteoblastic differentiation and contribute to the expression of alkaline phosphatase activity, a marker for fully differentiated osteoblastic cells.

Connexin mimetic peptides: specific inhibitors of gap-junctional intercellular communication

2001 ◽  
Vol 29 (4) ◽  
pp. 606-612 ◽  
Author(s):  
W. H. Evans ◽  
S. Boitano
Keyword(s):  
Gap Junctions ◽  
Intercellular Communication ◽  
Gap Junctional Intercellular Communication ◽  
Reversible Inhibitors ◽  
Gap Junctional Communication ◽  
Junctional Communication ◽  
Wide Range ◽  
Mimetic Peptides ◽  
Gap Junctional ◽  
Specific Sequences

Intercellular co-operation is a fundamental and widespread feature in tissues and organs. An important mechanism ensuring multicellular homoeostasis involves signalling between cells via gap junctions that directly connect the cytosolic contents of adjacent cells. Cell proliferation and intercellular communication across gap junctions are closely linked, and a number of pathologies in which communication is disrupted are known where connexins, the gap-junctional proteins, are modified. The proteins of gap junctions thus emerge as therapeutic targets inviting the development and exploitation of chemical tools and drugs that specifically influence intercellular communication. Connexin mimetic peptides that correspond to short specific sequences in the two extracellular loops of connexins are a class of benign, specific and reversible inhibitors of gap-junctional communication that have been studied recently in a broad range of cells, tissues and organs. This review summarizes the properties and uses of these short synthetic peptides, and compares their probable mechanism of action with those of a wide range of other less specific traditional gap-junction inhibitors.

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.

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