Knockdown of Transient Receptor Potential Canonical-1 Reduces the Proliferation and Migration of Endothelial Progenitor Cells

For this study, peripheral blood samples were collected from human volunteers. Mononuclear cells (MNC) were separated by density centrifugation and were induced to differentiate into endothelial progenitor cells (EPCs) in vitro. Different concentrations of rapamycin and silymarin were introduced to the EPCs over 24 hours and then EPCs were analyzed for proliferation, migration, apoptosis and angiogenesis. Compared with the control group, rapamycin (1, 10, 100 ng/mL) inhibited the proliferation and migration of EPCs in a concentration dependent manner ( P<0.05). Silymarin (50, 100 μg/mL) enhanced the proliferation and migration of EPCs and inhibited apoptosis in a concentration dependent manner ( P<0.05). By adding rapamycin (1 ng/mL) and silymarin (25, 50, 100 μg/mL) over 24 hours, silymarin inhibited the pro-apoptotic effect of rapamycin on EPCs, and reversed the inhibition of proliferation, migration and angiogenesis of EPCs by rapamycin ( P<0.05).

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Importance of melastatin-like transient receptor potential 7 and magnesium in the stimulation of osteoblast proliferation and migration by platelet-derived growth factor

AJP Cell Physiology ◽

10.1152/ajpcell.00614.2008 ◽

2009 ◽

Vol 297 (2) ◽

pp. C360-C368 ◽

Cited By ~ 85

Author(s):

Elie Abed ◽

Robert Moreau

Keyword(s):

Growth Factor ◽

Transient Receptor Potential ◽

Receptor Potential ◽

Platelet Derived Growth Factor ◽

Human Osteoblast ◽

Osteoblast Proliferation ◽

Transient Receptor ◽

And Migration ◽

Stimulation Of ◽

Proliferation And Migration

Bone is a dynamic tissue that is continuously being remodeled throughout life. Specialized cells called osteoclasts transiently break down old bone (resorption process) at multiple sites as other cells known as osteoblasts are replacing it with new tissue (bone formation). Usually, both resorption and formation processes are in balance and thereby maintain skeletal strength and integrity. This equilibrium is assured by the coordination of proliferation, migration, differentiation, and secretory functions of the osteoblasts, which are essential for adequate formation and resorption processes. Disturbances of this equilibrium may lead to decreased bone mass (osteoporosis), increased bone fragility, and susceptibility to fractures. Epidemiological studies have linked insufficient dietary magnesium (Mg2+) intake in humans with low bone mass and osteoporosis. Here, we investigated the roles of Mg2+ and melastatin-like transient receptor potential 7 (TRPM7), known as Mg2+ channels, in human osteoblast cell proliferation and migration induced by platelet-derived growth factor (PDGF), which has been involved in the bone remodeling process. PDGF promoted an influx of Mg2+, enhanced cell migration, and stimulated the gene expression of TRPM7 channels in human osteoblast MG-63 cells. The stimulation of osteoblast proliferation and migration by PDGF was significantly reduced under culture conditions of low extracellular Mg2+ concentrations. Silencing TRPM7 expression in osteoblasts by specific small interfering RNA prevented the induction by PDGF of Mg2+ influx, proliferation, and migration. Our results indicate that extracellular Mg2+ and TRPM7 are important for PDGF-induced proliferation and migration of human osteoblasts. Thus Mg2+ deficiency, a common condition among the general population, may be associated with altered osteoblast functions leading to inadequate bone formation and the development of osteoporosis.

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Transient receptor potential cation 3 channel regulates melanoma proliferation and migration

The Journal of Physiological Sciences ◽

10.1007/s12576-016-0480-1 ◽

2016 ◽

Vol 67 (4) ◽

pp. 497-505 ◽

Cited By ~ 13

Author(s):

Kayoko Oda ◽

Masanari Umemura ◽

Rina Nakakaji ◽

Ryo Tanaka ◽

Itaru Sato ◽

...

Keyword(s):

Transient Receptor Potential ◽

Receptor Potential ◽

Transient Receptor ◽

And Migration ◽

Proliferation And Migration

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Transient Receptor Potential Melastatin 8 (TRPM8) Channel Regulates Proliferation and Migration of Breast Cancer Cells by Activating the AMPK-ULK1 Pathway to Enhance Basal Autophagy

Frontiers in Oncology ◽

10.3389/fonc.2020.573127 ◽

2020 ◽

Vol 10 ◽

Author(s):

Yuan Huang ◽

Shi Li ◽

Zhenhua Jia ◽

Weiwei Zhao ◽

Cefan Zhou ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Transient Receptor Potential ◽

Receptor Potential ◽

Transient Receptor Potential Melastatin ◽

Ampk Activity ◽

Transient Receptor ◽

And Migration ◽

Proliferation And Migration

The calcium-permeable cation channel TRPM8 (transient receptor potential melastatin 8) is a member of the TRP superfamily of cation channels that is upregulated in various types of cancer with high levels of autophagy, including prostate, pancreatic, breast, lung, and colon cancers. Autophagy is closely regulated by AMP-activated protein kinase (AMPK) and plays an important role in tumor growth by generating nutrients through degradation of intracellular structures. Additionally, AMPK activity is regulated by intracellular Ca2+ concentration. Considering that TRPM8 is a non-selective Ca2+-permeable cation channel and plays a key role in calcium homoeostasis, we hypothesized that TRPM8 may control AMPK activity thus modulating cellular autophagy to regulate the proliferation and migration of breast cancer cells. In this study, overexpression of TRPM8 enhanced the level of basal autophagy, whereas TRPM8 knockdown reduced the level of basal autophagy in several types of mammalian cancer cells. Moreover, the activity of the TRPM8 channel modulated the level of basal autophagy. The mechanism of regulation of autophagy by TRPM8 involves autophagy-associated signaling pathways for activation of AMPK and ULK1 and phagophore formation. Impaired AMPK abolished TRPM8-dependent regulation of autophagy. TRPM8 interacts with AMPK in a protein complex, and cytoplasmic C-terminus of TRPM8 mediates the TRPM8–AMPK interaction. Finally, basal autophagy mediates the regulatory effects of TRPM8 on the proliferation and migration of breast cancer cells. Thus, this study identifies TRPM8 as a novel regulator of basal autophagy in cancer cells acting by interacting with AMPK, which in turn activates AMPK to activate ULK1 in a coordinated cascade of TRPM8-mediated breast cancer progression.

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NAMPT regulates senescence, proliferation, and migration of endothelial progenitor cells through the SIRT1 AS lncRNA/miR-22/SIRT1 pathway

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2016.08.133 ◽

2016 ◽

Vol 478 (3) ◽

pp. 1382-1388 ◽

Cited By ~ 32

Author(s):

Guang-feng Ming ◽

Kai Wu ◽

Kai Hu ◽

Yao Chen ◽

Jian Xiao

Keyword(s):

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Endothelial Progenitor ◽

And Migration ◽

Proliferation And Migration

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Estrogen induces endothelial progenitor cells proliferation and migration by estrogen receptors and PI3K-dependent pathways

Microvascular Research ◽

10.1016/j.mvr.2007.02.009 ◽

2008 ◽

Vol 75 (1) ◽

pp. 45-52 ◽

Cited By ~ 40

Author(s):

Xiaohui Zhao ◽

Lan Huang ◽

Yangguang Yin ◽

Yuqiang Fang ◽

Jinghong Zhao ◽

...

Keyword(s):

Estrogen Receptors ◽

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Endothelial Progenitor ◽

And Migration ◽

Proliferation And Migration

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Preliminary Study: Purple Sweet Potato Extract Seems to Be Superior to Increase the Migration of Impaired Endothelial Progenitor Cells Compared to l-Ascorbic Acid

Scientia Pharmaceutica ◽

10.3390/scipharm87030016 ◽

2019 ◽

Vol 87 (3) ◽

pp. 16

Author(s):

Yudi Her Oktaviono ◽

Makhyan Jibril Al-Farabi ◽

Luh Oliva Saraswati Suastika ◽

Febriyanti Hartono ◽

Yanni Dirgantara ◽

...

Keyword(s):

Ascorbic Acid ◽

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Sweet Potato ◽

Acid Treatment ◽

Endothelial Progenitor ◽

Treatment Dose ◽

Purple Sweet Potato ◽

And Migration ◽

Proliferation And Migration

Impairment of the endothelial progenitor cells (EPCs) ability to proliferate and migrate in the patients with coronary heart disease (CHD) is partly caused by oxidative stress. This research evaluates the effect of treatment with Ipomoea batatas L./purple sweet potato (PSP) extract and l-ascorbic acid on the proliferation and migration of impaired EPCs. EPCs were isolated from CHD patient’s peripheral blood. EPCs culture were cultivated and divided into control (untreated), PSP extract treatment (dose 1 and 25 μg/mL), and l-ascorbic acid treatment (dose 10 and 250 μg/mL) groups for 48 h. EPCs proliferation was analyzed with the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cell proliferation assay, and migration was evaluated with the cell migration assay kit. Statistical tests were evaluated using SPSS 25.0. This research showed that EPCs proliferation and migration was significantly higher in all PSP extract and l-ascorbic acid treatment compared to the control (p < 0.001). EPCs migration on treatment with a PSP extract dose of 25 μg/mL was significantly higher compared to the treatment with l-ascorbic acid dose of 250 μg/mL (303,000 ± 1000 compared to 215,000 ± 3000 cells, p< 0.001). In conclusion, both treatments with PSP extract and l-ascorbic acid can improve the proliferation and migration of impaired EPCs. At the dose of 25 μg/mL, PSP extract seems to be superior to the l-ascorbic acid dose of 250 μg/mL to improve EPCs migration.

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