Secretogranin III promotes angiogenesis through MEK/ERK signaling pathway

Tang, Fen; Pacheco, Mario Thiego Fernandes; Chen, Ping; Liang, Dan; Li, Wei

doi:10.1016/j.bbrc.2017.11.080

Cited by 18 publications

(17 citation statements)

References 25 publications

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“…Tang [5] et al conducted a related study on the pathway of SCG3 and found that blocking the MEK/ERK pathway inhibits the expression of SCG3. It was found that SCG3 and VEGF may have different receptor and signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

The research of Secretogranin III in periperal blood and vitreous of diabetic retinopathy

Jiao¹,

Sun²,

Wang³

et al. 2020

Preprint

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Background: Secretory granulin III (SCG3) is a member of the secretory granule protein family that regulates the production of secretory granules. SCG3 has a role in reducing retinal vascular leakage and neovascularization in an animal model of diabetic retinopathy. This study aimed to study SCG3 in periperal blood and vitreous of human. Methods ： (1) Collecting diabetic retinopathy(DR) patients required vitrectomy, and patients requiring vitrectomy for other non-diabetic factors, retaining some of the vitreous, ELISA was used to detect SCG3 in vitreous. The grouping was divided according to the patients’ blood lipids, BMI (Body Mass Index, BMI) and analyzed. (2) Collecting peripheral blood of DR and non-diabetic patients, ELISAwas performed. Results: (1) A total of 43 cases with DR were collected, and 34 cases non-diabetic patients were collected. SCG3 in DR patients was higher than that of non-diabetic. After refinement grouping, it was found that SCG3 with DR and hyperlipidemia was higher than that of non-diabetic patients without hyperlipidemia. SCG3 with DR and hyperlipidemia was higher than that of DR patients without hyperlipidemia. SCG3 of patients with DR and high BMI was higher than that of non-diabetic with normal BMI. SCG3 with DR and high BMI was higher than that of non-diabetic patients with normal BMI. (2) SCG3 in plasma was minimal or could not be detected. Conclusion： In DR patients, up-regulation of vitreous SCG3 may be closely related to the pathogenesis of DR. However, SCG3 is almost difficult to detect in normal vessel vasculature, which may highlight its advantages in using anti-SCG3 drugs in babies and children in future.

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Section: Discussionmentioning

confidence: 99%

The research of Secretogranin III in periperal blood and vitreous of diabetic retinopathy

Jiao¹,

Sun²,

Wang³

et al. 2020

Preprint

Self Cite

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“…Regarding the MAPK family members, increased activation of extracellular regulated protein kinase (ERK) can stimulate angiogenesis. The ERK signaling pathway plays a pivotal role in malignant processes, such as the development and proliferation of tumors and tumor angiogenesis . One study on prostate cancer showed that the RhoC/ROCK signaling pathway could upregulate the phosphorylation of MAPK, and the phosphorylation level of MAPK in prostate cancer tissues was significantly higher than that in adjacent tissues and was related to tumor cell metastasis .…”

Section: Discussionmentioning

confidence: 99%

“…The ERK signaling pathway plays a pivotal role in malignant processes, such as the development and proliferation of tumors and tumor angiogenesis. 10 One study on prostate cancer showed that the RhoC/ROCK signaling pathway could upregulate the phosphorylation of MAPK, and the phosphorylation level of MAPK in prostate cancer tissues was significantly higher than that in adjacent tissues and was related to tumor cell metastasis. 24 Therefore, with respect to the mechanisms through which VECs participate in angiogenesis, we focused on detecting phosphorylation of MAPK protein expression and found that the downregulation of RhoC interfered with phosphorylation of MAPK expression.…”

Section: Discussionmentioning

confidence: 99%

“…In angiogenesis studies, human umbilical vein endothelial cells (HUVECs) are usually selected as the model cell line. 10,11 Normal bone marrow plasma cells expressed more proangiogenic genes than antiangiogenic genes and induced angiogenesis in vitro. The accumulation of plasma cells can induce basal vascularization at the bone marrow level.…”

Section: Introductionmentioning

confidence: 99%

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Effects of RhoC downregulation on the angiogenesis characteristics of myeloma vascular endothelial cells

et al. 2019

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Background Tumor angiogenesis plays an important role in disease progression, and RhoC has been previously found to be expressed in vascular endothelial cells (VECs); however, its role in tumor angiogenesis requires clarification. This study aimed to explore the effects of RhoC downregulation on the cytoskeleton, pseudopod formation, migration ability, and canalization capacity of myeloma vascular endothelial cells (MVECs) in vitro. Materials and methods The expression of RhoC in MVECs and human umbilical vein endothelial cells (HUVECs) was knocked down by shRNA, and the expression levels of RhoC mRNA were detected by quantitative reverse transcription polymerase chain reaction (qRT‐PCR). The cytoskeletal changes and pseudopods were observed by laser scanning confocal and scanning electron microscopy; VECs were incubated in two‐dimensional Matrigel and three‐dimensional microcarriers to observe tube‐like structures and budding status, respectively. The protein expression of RhoC, phosphorylation of mitogen‐activated protein kinase (p‐MAPK), and Rho‐associated coiled‐coil kinase (ROCK) was determined by Western blotting. The expression of RhoC in VECs was downregulated by RhoC shRNA, thereby decreasing the number of pseudopods, two‐dimensional tube‐like structures, and buds. Results When RhoC was downregulated, the expression levels of ROCK and phosphorylation of MAPK were both decreased ( P < 0.05). Moreover, the expression levels of RhoC and phosphorylation of MAPK and three‐dimensional budding numbers were higher in MVECs than in HUVECs ( P < 0.05). The downregulation of RhoC expression in MVECs and HUVECs inhibited pseudopod formation, migration, canalization ability, and angiogenesis ( P < 0.05). Conclusion Our data indicated that MVECs and HUVECs were well suited for angiogenesis research, but the former cell type was shown to be more advantageous in terms of budding numbers. RhoC plays a pivotal role in MVECs angiogenesis, and the downregulation of RhoC expression could inhibit angiogenesis via the RhoC/MAPK and RhoC/ROCK signaling pathways.

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“…Human umbilical vein endothelial cells (7 × 10 4 cells/well) were suspended and seeded in matrigel-coated (100 μL/well) 48-well plates. NF-κB inhibitor BAY 11-7082 (500 nmol/L), Erk-MAPK inhibitor SCH772984 (250 nmol/L), p38-MAPK inhibitor SB 202190 (1 μmol/L), and VEGF antagonist sFlt-1 (2.5 μmol/L) ( Berger et al, 2012 ; Pan et al, 2015 ; Gu et al, 2017 ; Tang et al, 2018 ), at non-toxic concentrations were added to RPE cells, from which CM was collected to treat HUVECs in order to unravel the possible anti-AMD mechanism of Kin. After 8 h, HUVECs were stained with calcein-AM (2 μmol/L), and tube formation was observed under confocal microscopy.…”

Section: Methodsmentioning

confidence: 99%

Kinsenoside Ameliorates Oxidative Stress-Induced RPE Cell Apoptosis and Inhibits Angiogenesis via Erk/p38/NF-κB/VEGF Signaling

Luo¹,

Gu²,

Zhang³

et al. 2018

Front. Pharmacol.

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The pathological superoxidative condition that retinal pigment epithelium (RPE) cells experience contributed to the advancement of age-related macular degeneration (AMD), which was accompanied by significant neovascularization. Therefore, the discovery of novel pharmacological candidates to ameliorate oxidative damage (H2O2) against RPE cells and inhibit the following angiogenesis simultaneously is urgently needed. Herein, we found that kinsenoside (Kin), an active component derived from Anoectochilus roxburghii, was able to protect RPE cells effectively and attenuate subsequent angiogenesis. In this study, H2O2-induced oxidative injury reduced RPE cell viability and increased cell apoptosis, which was significantly rescued by the treatment with Kin. Compared with H2O2 alone, Kin decreased the levels of Bax and increased the production of Bcl-2 in RPE cells. H2O2-stimulated VEGF up-regulation was inhibited by Kin treatment. Human umbilical vein endothelial cell (HUVEC) neovascularization induced by conditioned medium (CM) from H2O2-stimulated RPE cells was attenuated by treatment with Kin, VEGF antagonist, NF-κB, Erk-MAPK, and p38-MAPK inhibitors. Additionally, H2O2-activated phosphorylated expression of IκBα, p65, Erk, and p38 in RPE cells was inhibited by treatment with Kin. Taken together, Kin protected RPE from apoptosis against oxidative stress while simultaneously decreasing apoptosis-related neovascularization. This could be ascribed to the inhibition of Erk/p38/NF-κB signaling by Kin that contributed to the resulting decreased VEGF expression in H2O2-treated RPE cells.

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Secretogranin III promotes angiogenesis through MEK/ERK signaling pathway

Cited by 18 publications

References 25 publications

The research of Secretogranin III in periperal blood and vitreous of diabetic retinopathy

The research of Secretogranin III in periperal blood and vitreous of diabetic retinopathy

Effects of RhoC downregulation on the angiogenesis characteristics of myeloma vascular endothelial cells

Kinsenoside Ameliorates Oxidative Stress-Induced RPE Cell Apoptosis and Inhibits Angiogenesis via Erk/p38/NF-κB/VEGF Signaling

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