Human Gastric Smooth Muscle Cells (HGSMC)

Cat.No.: CSC-7779W

Species: Human

Source: Stomach

Cell Type: Smooth Muscle Cell

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Cat.No.
CSC-7779W
Description
Smooth muscle is responsible for the contractility of hollow organs, such as blood vessels, the gastrointestinal tract, the bladder, and the uterus. Its structure differs greatly from that of skeletal muscle. The human stomach contains three layers of muscle in its walls, the outer longitudinal, the middle circular and the inner oblique and visceral smooth muscle cells makes up all three layers along the entire organ. Smooth muscle contraction is critical to peristalsis in the human stomach and the contraction may be mediated by activation of phospholipase through two distinct mechanisms (increased intracellular Ca2+ and G protein activation) and activating PKCepsilon-dependent mechanisms. In vitro study also shows that gastric smooth muscle cells express ET and eNOS and both calcium and sodium may be involved as current carriers in the generation of the plateau potential.HGSMC from Bioarray Research Laboratories are isolated from the human stomach. HGSMC are cryopreserved at secondary culture and delivered frozen. Each vial contains >5 x 10^5 cells in 1 ml volume. HGSMC are characterized by immunofluorescent method with antibodies to Α-smooth muscle actin and desmin. HGSMC are negative for HIV-1, HBV, HCV, mycoplasma, bacteria, yeast and fungi. HGSMC are guaranteed to further expand for 15 population doublings at the condition provided by Bioarray Research Laboratories.
Species
Human
Source
Stomach
Cell Type
Smooth Muscle Cell
Disease
Normal
Storage and Shipping
Directly and immediately transfer cells from dry ice to liquid nitrogen upon receiving and keep the cells in liquid nitrogen until cell culture needed for experiments.
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

Human gastric smooth muscle cells (HGSMC) are primary cells isolated from human stomach tissue that provide a physiologically relevant in vitro model system for studying gastric motility as well as other smooth muscle-mediated gastrointestinal functions. HGSMCs maintain many structural, molecular, and functional properties of gastric smooth muscle cells in vivo. HGSMCs are spindle-shaped elongated cells that attach and proliferate as monolayers under conventional culture conditions. They also express several smooth muscle specific proteins such as α-smooth muscle actin (α-SMA), smooth muscle myosin heavy chain, calponin, and desmin. Functionally, HGSMCs contract and relax in response to neural and hormonal regulators of gastric motility, including acetylcholine (muscarinic receptors), nitric oxide-dependent relaxation pathways, and calcium-induced contraction.

HGSMCs are commonly utilized to explore basic mechanisms underlying diseases associated with gastric motility dysfunction, such as gastroparesis, functional dyspepsia, and inflammatory-induced gastric smooth muscle cell dysfunction. Furthermore, they serve as an excellent cell model for screening prokinetic/antispasmodic drug candidates, as well as studying smooth muscle proliferation, phenotype switching, and extracellular matrix remodeling.

Maslinic Acid Improves Mitochondrial Function and Inhibits Oxidative Stress and Autophagy in Human Gastric Smooth Muscle Cells

Functional dyspepsia (FD) is a common chronic gastroduodenal disorder lacking efficient pharmacotherapy. Zheng's team explored if maslinic acid (MA), pentacyclic triterpene acid extracted from hawthorn, exerted cytoprotection on human gastric smooth-muscle cells (HGSMCs) against mitochondrial damage and further investigated the mechanisms involved.

Figure 1a displayed the chemical structure of MA. After that, we found that cell viability was progressively augmented after treatment with MA (20, 40, 80 and 160 μM), and then 20, 40 and 80 μM MA treatments were selected for subsequent studies (Fig. 1b). Taken together, MA promoted cell viability in HGSMCs. They found that the ATP level was decreased after CCCP induction while this decrease was abrogated after MA treatment (20, 40 and 80 μM) (Fig. 2a). Additionally, the MMP levels decreased after CCCP addition, but this effect was reversed after MA treatment (Fig. 2b). Taken together, MA ameliorated mitochondrial function in HGSMCs. The protein expression of LC3II/LC3I was increased and that of P62 was attenuated after CCCP stimulation, but these impacts were counteracted after MA addition (Fig. 3a). Moreover, the LC3B fluorescence intensity was heightened after CCCP induction, but this increase was neutralized after MA treatment (Fig. 3a and b). Overall, MA restrained autophagy in HGSMCs.

MA accelerated cell viability of HGSMCs.

Fig. 1. MA accelerated cell viability of HGSMCs (Zheng X Y, Zhang S, et al., 2025).

MA ameliorated mitochondrial function in HGSMCs.

Fig. 2. MA ameliorated mitochondrial function in HGSMCs (Zheng X Y, Zhang S, et al., 2025).

MA restrained autophagy in HGSMCs.

Fig. 3. MA restrained autophagy in HGSMCs (Zheng X Y, Zhang S, et al., 2025).

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