Trabecular Meshwork Cell Medium

Name: Trabecular Meshwork Cell Medium
Brand: Sciencell Research Laboratories
SKU: 6591
Price: 146 USD
Availability: InStock

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Catalog No.

6591

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$146.00

Trabecular Meshwork Cell Medium (TMCM) consists of 500 ml of basal medium, 10 ml of FBS (Cat. #0010), 5 ml of Trabecular Meshwork Cell Growth Supplement (TMCGS, Cat. #6592) and 5 ml of penicillin/streptomycin solution (P/S, Cat. #0503).

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Trabecular Meshwork Cell Medium (TMCM), when used with Trabecular Meshwork Cell Growth Supplement (TMCGS, Cat #6592) and 10 ml of fetal bovine serum (FBS) is a complete medium designed for optimal growth of normal trabecular meshwork cells in vitro. It is a sterile, liquid medium which contains essential and non-essential amino acids, vitamins, organic and inorganic compounds, hormones, growth factors, trace minerals and a low concentration of fetal bovine serum (2%). The medium is HEPES and bicarbonate buffered and has a pH of 7.4 when equilibrated in an incubator with an atmosphere of 5% CO2/95% air. The medium is formulated (quantitatively and qualitatively) to provide an optimally balanced nutritional environment that selectively supports the growth of normal trabecular meshwork cells in vitro.

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Catalog No.	6591
Product Code	TMCM
Size/Quantity	500 ml
Product use	This product is for research use only. It is not approved for use in humans, animals, or in vitro diagnostic procedures.
Storage	Store the basal medium at 4°C, the TMCGS, the FBS and the P/S solution at -20°C. Protect from light.
Shipping	Basal medium: room temperature. Supplements: dry ice.

1. Yue Wan, Xiangxiang Liu, Xuejing Yan, Shen Wu, Yufei Teng, Luyi Han, Jingxue Zhang, Ningli Wang; AAV-DJ–Mediated MYOC Silencing as a Gene Therapy Approach for Myocilin-Associated Glaucoma. Invest. Ophthalmol. Vis. Sci. 2026;67(1):48. https://doi.org/10.1167/iovs.67.1.48.

Purpose: To evaluate the therapeutic efficacy of an adeno-associated virus serotype DJ (AAV-DJ) vector delivering MYOC-targeting short-hairpin RNA (shMYOC) in a MYOCP370... More

2. Yu, N., Zhang, Z., Chen, P., Zhong, Y., Cai, X., Hu, H., Yang, Y., Zhang, J., Li, K., Ge, J., Yu, K., Liu, X. & Zhuang, J. (2015) Tetramethylpyrazine (TMP), an Active Ingredient of Chinese Herb Medicine Chuanxiong, Attenuates the Degeneration of Trabecular Meshwork through SDF-1/CXCR4 Axis PLoS One. 10

Background A traditional Chinese medicine, Tetramethylpyrazine (TMP), has been prescribed as a complementary treatment for glaucoma to improve patient prognosis. However,... More

Background A traditional Chinese medicine, Tetramethylpyrazine (TMP), has been prescribed as a complementary treatment for glaucoma to improve patient prognosis. However, the pharmacological mechanism of action of TMP is poorly understood. In previous studies, we demonstrated that TMP exerts potent inhibitory effects on neovascularization, suppresses the tumorigenic behavior of glioma cells, and protects neural cells by regulating CXCR4 expression. Here, we further investigated whether the SDF-1/CXCR4 pathway is also involved in the TMP-mediated activity in trabecular meshwork cells. Methodology/Principal Findings CXCR4 expression was examined by quantitative real-time PCR in trabecular and iris specimens from 54 primary open-angle glaucoma (POAG) patients who required surgery and 19 non-glaucomatous donors. Our data revealed markedly elevated CXCR4 expression in the trabecular meshwork of POAG patients compared with that of controls. Consistently, CXCR4 expression was much higher in glaucomatous trabecular meshwork cells than in normal trabecular meshwork cells. Using RT-PCR and western blot assays, we determined that glaucoma-related cytokines and dexamethasone (DEX) also significantly up-regulated CXCR4 expression in primary human trabecular meshwork (PHTM) cells. Moreover, the TGF-β1-mediated induction of CXCR4 expression in PHTM cells was markedly down-regulated by TMP compared with control treatment (PBS) and the CXCR4 antagonist AMD3100. In addition, TMP could counteract the TGF-β1-induced effects on stress fiber accumulation and expansion of PHTM cells. TMP markedly suppressed the migration of PHTM cells stimulated by TGF-β1 in transwell and scratch wound assays. TMP also suppressed the extracellular matrix (ECM) accumulation induced by TGF-β2. Conclusions Our findings demonstrate that CXCR4 might be involved in the pathogenetic changes in the trabecular meshwork of patients with POAG. Additionally, TMP might exert its beneficial effects in POAG patients by down-regulating CXCR4 expression. Less

ScienCell Research Laboratories (SRL) takes pride in being a resource for researchers all over the world. The publications listed here are not meant as an endorsement or confirmation of the reliability of the products.