Enhancing action by sulfated hyaluronan on connexin‐26, ‐32, and ‐43 gene expressions during the culture of normal human astrocytes

Ahmed, Saifuddin; Tsuchiya, Toshie; Nagahata-Ishiguro, Misao; Sawada, Rumi; Banu, Nasreen; Nagira, Tsutomu

doi:10.1002/jbm.a.32018

Cited by 3 publications

(2 citation statements)

References 22 publications

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“…Sulfated hyaluronan can increase proliferation of normal human astrocytes and differentiation through enhanced expression of connexin-26, -32, and -43 [83]. Hyaluronan-containing hydrogels provide a suitable environment for neural stem cell growth and differentiation [84, 85].…”

Section: Hyaluronan Regulates Tissue Morphogenesismentioning

confidence: 99%

Hyaluronan Regulates Cell Behavior: A Potential Niche Matrix for Stem Cells

Solís

Chen

Wong

et al. 2012

Biochemistry Research International

178

114

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Hyaluronan is a linear glycosaminoglycan that has received special attention in the last few decades due to its extraordinary physiological functions. This highly viscous polysaccharide is not only a lubricator, but also a significant regulator of cellular behaviors during embryogenesis, morphogenesis, migration, proliferation, and drug resistance in many cell types, including stem cells. Most hyaluronan functions require binding to its cellular receptors CD44, LYVE-1, HARE, layilin, and RHAMM. After binding, proteins are recruited and messages are sent to alter cellular activities. When low concentrations of hyaluronan are applied to stem cells, the proliferative activity is enhanced. However, at high concentrations, stem cells acquire a dormant state and induce a multidrug resistance phenotype. Due to the influence of hyaluronan on cells and tissue morphogenesis, with regards to cardiogenesis, chondrogenesis, osteogenesis, and neurogenesis, it is now been utilized as a biomaterial for tissue regeneration. This paper summarizes the most important and recent findings regarding the regulation of hyaluronan in cells.

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Section: Hyaluronan Regulates Tissue Morphogenesismentioning

confidence: 99%

Hyaluronan Regulates Cell Behavior: A Potential Niche Matrix for Stem Cells

Solís

Chen

Wong

et al. 2012

Biochemistry Research International

178

114

View full text Add to dashboard Cite

show abstract

“…The impact of DAMPs on connexin expression is more divergent than PAMPs ( Table 1 ). For instance, an increase in the expression of connexins, such as Cx26, Cx32 and Cx43, can be induced by the application of DAMPs, such as biglycan, versican, hyaluronan, heparan, fibronectin and high-mobility group box-1 (HMGB1), in fibroblast, astrocytes and alveolar epithelial cells [ 66 , 67 , 68 , 69 , 70 , 71 , 72 ]. Conversely, other DAMPs, such as uric acid and heat-shock proteins, can suppress the expression of Cx26 and Cx43 in astrocytes, cardiac myocytes, vascular endothelial and colorectal cancer cells [ 73 , 74 ].…”

Section: Association Of Cxhc With Pathogenesis Of Inflammatory Diseasesmentioning

confidence: 99%

The Role of Connexin Hemichannels in Inflammatory Diseases

Peng

Wang

et al. 2022

Biology

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The connexin protein family consists of approximately 20 members, and is well recognized as the structural unit of the gap junction channels that perforate the plasma membranes of coupled cells and, thereby, mediate intercellular communication. Gap junctions are assembled by two preexisting hemichannels on the membranes of apposing cells. Non-junctional connexin hemichannels (CxHC) provide a conduit between the cell interior and the extracellular milieu, and are believed to be in a protectively closed state under physiological conditions. The development and characterization of the peptide mimetics of the amino acid sequences of connexins have resulted in the development of a panel of blockers with a higher selectivity for CxHC, which have become important tools for defining the role of CxHC in various biological processes. It is increasingly clear that CxHC can be induced to open by pathogen-associated molecular patterns. The opening of CxHC facilitates the release of damage-associated molecular patterns, a class of endogenous molecules that are critical for the pathogenesis of inflammatory diseases. The blockade of CxHC leads to attenuated inflammation, reduced tissue injury and improved organ function in human and animal models of about thirty inflammatory diseases and disorders. These findings demonstrate that CxHC may contribute to the intensification of inflammation, and serve as a common target in the treatments of various inflammatory diseases. In this review, we provide an update on the progress in the understanding of CxHC, with a focus on the role of these channels in inflammatory diseases.

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Targeting Hyaluronidase for Cancer Therapy: Antitumor Activity of Sulfated Hyaluronic Acid in Prostate Cancer Cells

et al. 2011

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The tumor cell-derived hyaluronidase HYAL-1 degrades hyaluronic acid (HA) into pro-angiogenic fragments that support tumor progression. Although HYAL-1 is a critical determinant of tumor progression and a marker for cancer diagnosis and metastasis prediction, it has not been evaluated as a target for cancer therapy. Similarly, sulfated hyaluronic acid (sHA) has not been evaluated for biological activity, although it is a HAase inhibitor. In this study we show that sHA is a potent inhibitor of prostate cancer. sHA blocked the proliferation, motility and invasion of LNCaP, LNCaP-AI, DU145 and LAPC-4 prostate cancer cells, also inducing caspase 8-dependent apoptosis associated with downregulation of Bcl-2 and phospho-Bad. sHA inhibited Akt signaling including androgen receptor (AR) phosphorylation, AR-activity, NFkb activation and VEGF expression. These effects were traced to a blockade in complex formation between PI3K and HA receptors and to a transcriptional downregulation of HA receptors, CD44 and RHAMM, along with PI3K inhibition. Angiogenic HA fragments or overexpression of myristoylated-Akt or HA receptors blunted these effects of sHA, implicating a feedback loop between HA receptors and PI3K/Akt signaling in the mechanism of action. In an animal model, sHA strongly inhibited LNCaP-AI prostate tumor growth without causing weight loss or apparent serum-organ toxicity. Inhibition of tumor growth was accompanied by a significant decrease in tumor angiogenesis and an increase in apoptosis index. Taken together, our findings offer mechanistic insights into the tumor-associated HA-HAase system and a preclinical proof-of-concept of the safety and efficacy of sHA to control prostate cancer growth and progression.

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Enhancing action by sulfated hyaluronan on connexin‐26, ‐32, and ‐43 gene expressions during the culture of normal human astrocytes

Cited by 3 publications

References 22 publications

Hyaluronan Regulates Cell Behavior: A Potential Niche Matrix for Stem Cells

Hyaluronan Regulates Cell Behavior: A Potential Niche Matrix for Stem Cells

The Role of Connexin Hemichannels in Inflammatory Diseases

Targeting Hyaluronidase for Cancer Therapy: Antitumor Activity of Sulfated Hyaluronic Acid in Prostate Cancer Cells

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