Induced differentiation of human gingival fibroblasts into VSMC-like cells

Liu, Xuqian; Wang, Jie; Fang, Dong; Li, Hexiang; Hou, Yuchuan

doi:10.1016/j.diff.2017.01.001

Cited by 10 publications

(12 citation statements)

References 39 publications

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“…Findings of the present study are consistent with the previous studies, which reported that the inhibition of PI3K dramatically alleviates inflammatory and neuropathic pain 19,20,30. Several studies have demonstrated that RES can reverse mitochondrial damage against oxidative stress-induced neuronal death through the activation of PI3K/Akt signaling pathway 2,24. In vivo researches reported that PI3K inhibitor, LY29400, can significantly reduce the level of spinal microglia in animal model of bone cancer pain 20…”

Section: Discussionsupporting

confidence: 91%

“…The phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) pathway is one of the most important participants in modulating nociceptive information and is centrally sensitized in the microglial intracellular signaling cascades 25. RES has been found to protect neuronal cells from oxidative cytotoxicity via PI3K/Akt pathway 24. However, the potential mechanism of RES in preventing paclitaxel-induced neuropathic pain has yet to be explored.…”

Section: Introductionmentioning

confidence: 99%

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<p>Resveratrol inhibits paclitaxel-induced neuropathic pain by the activation of PI3K/Akt and SIRT1/PGC1α pathway</p>

Li¹,

Yang²,

Wang³

et al. 2019

JPR

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Background Phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) is one of the essential signaling pathways for the development and maintenance of neuropathic pain. Objective To investigate the effect of resveratrol (RES) on paclitaxel-induced neuropathic pain in rats and elucidate the underlying molecular mechanisms. Method Male Sprague Dawley rats were randomly divided into seven groups (n=10/group): Group C, Group P, Group R, Group R+P, Group LY + R+P, Group LY (the specific inhibitor of PI3K), Group E (the specific inhibitor of sirtuin 1 [SIRT1]). Paw withdrawal mechanical threshold (PWT) and thermal withdrawal latency (TWL) were recorded. Mitochondrial histomorphology was performed by transmission electron microscope. PI3K, p-Akt, and t-Akt expressions were tested using immunohistochemistry. Western blot was used to detect p-Akt, t-Akt, SIRT1, and PGC1α expressions. The apoptosis in the striatum, spinal dorsal horns (SDH), and dorsal root ganglions (DRG) tissues was assayed by TUNEL. ELISA was used to detect the contents of IL-β, IL-10, malondialdehyde (MDA), and superoxide dismutase (SOD) in striatum, SDH, and DRG tissues. Results Compared to the control group, PWT and TWL in the P and LY +R+P groups were significantly decreased on 8th and 14th day after paclitaxel administration ( P <0.05). The expressions of p-Akt, SIRT1, and PGC1α were decreased in paclitaxel-induced neuropathic rats; however, the expressions of p-Akt, SIRT1, and PGC1α were significantly increased after RES treatment ( P <0.05). Furthermore, the expression of p-Akt was decreased by LY294002 ( P <0.05), and amount of SIRT1 and PGC1α expression was inhibited by EX-527 ( P <0.05). The t-Akt level was not significantly changed in all groups. RES prevented paclitaxel-induced mitochondrial damage by PI3K/Akt. RES improves the pain symptoms of paclitaxel neuralgia rats by increasing the IL-10 and decreasing the expression of IL-1β. RES increases the SOD and reduces the MDA. RES reduces apoptosis by SIRT1/PGC1α signal pathway. Conclusion Our results suggest that RES may inhibit paclitaxel-induced neuropathic pain via PI3K/Akt and SIRT1/PGC1α pathways.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

<p>Resveratrol inhibits paclitaxel-induced neuropathic pain by the activation of PI3K/Akt and SIRT1/PGC1α pathway</p>

Li¹,

Yang²,

Wang³

et al. 2019

JPR

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“…HGFs were used for cell studies. HGFs were isolated from healthy gingival tissue, which was harvested from clinical donors undergoing mandibular third impact molar extraction as described previously (30). The acquisition of normal human gingival tissues from patients was approved by the Hospital of Stomatology at Hebei Medical University (Hebei, China), and written informed consent was obtained from all patients.…”

Section: Methodsmentioning

confidence: 99%

Characterization of different biodegradable scaffolds in tissue engineering

et al. 2019

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The aim of the present study was to compare the characteristics of acellular dermal matrix (ADM), small intestinal submucosa (SIS) and Bio-Gide scaffolds with acellular vascular matrix (ACVM)-0.25% human-like collagen I (HLC-I) scaffold in tissue engineering blood vessels. The ACVM-0.25% HLC-I scaffold was prepared and compared with ADM, SIS and Bio-Gide scaffolds via hematoxylin and eosin (H&E) staining, Masson staining and scanning electron microscope (SEM) observations. Primary human gingival fibroblasts (HGFs) were cultured and identified. Then, the experiment was established via the seeding of HGFs on different scaffolds for 1, 4 and 7 days. The compatibility of four different scaffolds with HGFs was evaluated by H&E staining, SEM observation and Cell Counting Kit-8 assay. Then, a series of experiments were conducted to evaluate water absorption capacities, mechanical abilities, the ultra-microstructure and the cytotoxicity of the four scaffolds. The ACVM-0.25% HLC-I scaffold was revealed to exhibit the best cell proliferation and good cell architecture. ADM and Bio-Gide scaffolds exhibited good mechanical stability but cell proliferation was reduced when compared with the ACVM-0.25% HLC-I scaffold. In addition, SIS scaffolds exhibited the worst cell proliferation. The ACVM-0.25% HLC-I scaffold exhibited the best water absorption, followed by the SIS and Bio-Gide scaffolds, and then the ADM scaffold. In conclusion, the ACVM-0.25% HLC-I scaffold has good mechanical properties as a tissue engineering scaffold and the present results suggest that it has better biological characterization when compared with other scaffold types.

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“…Prior to vascular grafting, the tissue capsules were composed primarily of fibroblasts, myofibroblasts, and collagen. Fibroblasts are characterized by remarkable plasticity [17][18][19], with the ability to differentiate into VSMCs [20]. Even though the initial tissue capsule was composed almost entirely of fibroblasts and numerous luminal macrophages, within a month of vascular grafting the tissue capsules began to show a notable increase in desmin-positive VSMC-like cells, as well as a notable decrease in macrophages.…”

Section: Discussionmentioning

confidence: 99%

A novel method for engineering autologous non-thrombogenic in situ tissue-engineered blood vessels for arteriovenous grafting

et al. 2020

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Induced differentiation of human gingival fibroblasts into VSMC-like cells

Cited by 10 publications

References 39 publications

<p>Resveratrol inhibits paclitaxel-induced neuropathic pain by the activation of PI3K/Akt and SIRT1/PGC1α pathway</p>

<p>Resveratrol inhibits paclitaxel-induced neuropathic pain by the activation of PI3K/Akt and SIRT1/PGC1α pathway</p>

Characterization of different biodegradable scaffolds in tissue engineering

A novel method for engineering autologous non-thrombogenic in situ tissue-engineered blood vessels for arteriovenous grafting

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Induced differentiation of human gingival fibroblasts into VSMC-like cells

Cited by 10 publications

References 39 publications

<p>Resveratrol inhibits paclitaxel-induced neuropathic pain by the activation of PI3K/Akt and SIRT1/PGC1&alpha; pathway</p>

<p>Resveratrol inhibits paclitaxel-induced neuropathic pain by the activation of PI3K/Akt and SIRT1/PGC1&alpha; pathway</p>

Characterization of different biodegradable scaffolds in tissue engineering

A novel method for engineering autologous non-thrombogenic in situ tissue-engineered blood vessels for arteriovenous grafting

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<p>Resveratrol inhibits paclitaxel-induced neuropathic pain by the activation of PI3K/Akt and SIRT1/PGC1α pathway</p>

<p>Resveratrol inhibits paclitaxel-induced neuropathic pain by the activation of PI3K/Akt and SIRT1/PGC1α pathway</p>