Hormonal, pH, and Calcium Regulation of Connexin 43–Mediated Dye Transfer in Osteocytes in Chick Calvaria

Ishihara, Yoshihito; Kamioka, Hiroshi; Honjo, Tadashi; Ueda, Hirotaka; Takano‐Yamamoto, Teruko; Yamashiro, Takashi

doi:10.1359/jbmr.071102

Cited by 49 publications

(33 citation statements)

References 63 publications

(68 reference statements)

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“…Connexin isoforms found in the hamster cheek pouch tissue include Cx 37, 40 and 43 [59]. Some studies report that 18αGA transiently blocks Cx 43 [60,61,62], but also may block other gap junctions, such as Cx 27 [62]. This may suggest that Cx 43 may be required for the FGF but not VEGF response.…”

Section: Discussionmentioning

confidence: 99%

Downstream Exposure to Growth Factors Causes Elevated Velocity and Dilation in Arteriolar Networks

2010

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Our goal was to characterize changes in flow and diameter with vascular endothelial cell growth factor A (VEGF-A) and fibroblast growth factor 2 (FGF2). Observations were made in arteriolar networks of the cheek pouch tissue in anesthetized hamsters (pentobarbital 70 mg/kg, i.p., n = 45). Local and remote dilation responses to micropipette-applied VEGF or FGF2 yielded similar EC₅₀ values. The role of gap junctions in the remote response was tested by applying sucrose, halothane or 18αGA to the feed arteriole midway between the remote stimulation and upstream observation sites; all remote dilation to FGF2 was prevented, while only the early dilation to VEGF was blocked. The remote dilation to VEGF displayed a second rheologic mechanism. The second mechanism involved an abrupt increase in upstream velocity and shear rate, followed by nitro-arginine sensitive dilation. To test whether the abrupt increase in shear could be caused by other agents known to cause edema, remote responses to histamine and thrombin were tested. Each caused an abrupt increase in velocity followed by nitro-arginine-sensitive dilation. This study shows that VEGF or agents that increase permeability can initiate an upstream velocity increase with dilation that recruits flow to the network; this is in addition to simultaneous gap junction-mediated dilation.

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Section: Discussionmentioning

confidence: 99%

Downstream Exposure to Growth Factors Causes Elevated Velocity and Dilation in Arteriolar Networks

2010

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“…Because osteocytes communicate with each other through the gap junction [23], we next explored the influence of substrate stiffness on the gap junction by examining connexin 43, whose distribution is reported in vitro [24] and in vivo [25]. At the protein level, we first found an interaction between paxillin and connexin 43 by Co-IP (Fig.…”

Section: Substrate Stiffness Modulates the Gap Junction Elongation Ofmentioning

confidence: 99%

Extracellular Matrix Elasticity Regulates Osteocyte Gap Junction Elongation: Involvement of Paxillin in Intracellular Signal Transduction

Zhang

Zhou

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Osteocytes can sense and respond to extracellular stimuli, including biochemical factors throughout the cell body, dendritic processes, and cilia bending. However, further exploration is required of osteocyte function in response to substrate stiffness, an important passive mechanical cue at the interface between osteocytes and the extracellular matrix, and the deep bio-mechanism in osteocytes involving mechanosensing of cell behavior. Methods: We fabricated silicon-based elastomer polydimethylsiloxane substrates with different stiffnesses but with the same surface topologies. We then seeded osteocytes onto the substrates to examine their responses. Methodologies used included scanning electron microscopy (SEM) for cell morphology, confocal laser scanning microscopy (CLSM) for protein distribution, western blot for protein levels, co-immunoprecipitation for protein interactions, and quantitative real-time polymerase chain reaction for gene expression. Results: SEM images revealed that substrate stiffness induced a change in osteocyte morphology, and CLSM of F-actin staining revealed that substrate stiffness can alter the cytoskeleton. These results were accompanied by changes in focal adhesion capacity in osteocytes, determined via characterization of vinculin expression and distribution. Furthermore, on the exterior of the cell membrane, fibronectin was altered by substrate stiffness. The fibronectin then induced a change in paxillin on the inner membrane of the cell via protein–protein interaction through transmembrane processing. Paxillin led to changes in connexin 43 via protein–protein binding, thereby influencing osteocyte gap junction elongation. Conclusion: This process -from mechanosensing and mechanotransduction to cell function - not only indicates that the effects of mechanical factors on osteocytes can be directly sensed from the cell body, but also indicates the involvement of paxillin transduction.

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“…1) [12][13][14]. Recent data have proven in ex-vivo calvaria organ cultures that gap junctions allow cell-cell communication among the osteocytic network, and that such communication is regulated by parathyroid hormone (PTH) and pH [15]. Connexins are involved in many aspects of bone cell function, including control of osteoblastic cell proliferation [16;17] differentiation [18][19][20] and survival [21].…”

Section: Connexins and Cell-cell Communicationmentioning

confidence: 99%

Cell–cell communication in the osteoblast/osteocyte lineage

Civitelli

2008

Archives of Biochemistry and Biophysics

228

174

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Skeletal development (bone modeling) and its maintenance in post-natal life in response to local and systemic stimuli (bone remodeling) require coordinated activity among osteoblasts (bone forming cells), osteocytes (cells embedded in bone) and osteoclasts (bone resorbing cells), in order to meet the needs of structural integrity, mechanical competence and maintenance of mineral homeostasis. One mechanism of cell-cell interaction is via direct cell-cell communication via gap junctions. These are transmembrane channels that allow continuity of cytoplasms between communicating cells. The biologic importance of connexin43 (Cx43), the most abundant gap junction protein in the skeleton is demonstrated by the skeletal malformations present in oculodentodigital dysplasia (ODDD), a disease linked to Cx43 gene (GJA1) mutations, and by the low bone mass and osteoblast dysfunction in Gja1 ablated mice. The presence of Cx43 is required for osteoblast differentiation and function, and by forming either gap junctions or "hemichannels" Cx43 allows participation of cell networks to responses to extracellular stimuli, via propagation of specific signals converging upon connexin sensitive transcriptional units. Hence, Cx43 is involved in skeletal responsiveness to anabolic signals, as those provided by parathyroid hormone and physical load, the latter function probably involving osteocyte-osteoblast communication.

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Hormonal, pH, and Calcium Regulation of Connexin 43–Mediated Dye Transfer in Osteocytes in Chick Calvaria

Cited by 49 publications

References 63 publications

Downstream Exposure to Growth Factors Causes Elevated Velocity and Dilation in Arteriolar Networks

Downstream Exposure to Growth Factors Causes Elevated Velocity and Dilation in Arteriolar Networks

Extracellular Matrix Elasticity Regulates Osteocyte Gap Junction Elongation: Involvement of Paxillin in Intracellular Signal Transduction

Cell–cell communication in the osteoblast/osteocyte lineage

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