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Streptozotocin?induced diabetic mice exhibit reduced experimental choroidal neovascularization but not corneal neovascularization.

ABSTRACT: The present study aimed to investigate the effects of diabetes mellitus (DM) on the generation of experimental corneal neovascularization (CrNV) and choroidal neovascularization (ChNV). Diabetes was induced in mice by intraperitoneal injection of streptozotocin (STZ). Experimental CrNV and ChNV were induced by alkali injury and laser photocoagulation, respectively. CrNV and ChNV were compared between the STZ?induced diabetic mice and control mice two weeks after injury. Relative expression of angiogenic factors was quantified by reverse transcription?quantitative polymerase chain reaction, and progenitor cell or macrophage accumulation in the early phase following injury was examined by flow cytometric analysis. Compared with the alkali?injured normal mice, the alkali?injured diabetic mice (STZ?induced) exhibited no significant difference in CrNV occurrence, whereas the laser?injured diabetic mice exhibited significantly reduced levels of ChNV compared with those of the laser?injured control animals. The laser?induced intrachoroidal mRNA expression levels of angiogenic factors, including vascular endothelial growth factor, hypoxia?induced factor?1?, chemokine (C?C motif) ligand 3, and stromal cell?derived factor?1?, were reduced in the laser?injured diabetic mice when compared with laser?injured control mice. Furthermore, the laser?induced intrachoroidal infiltration of c?Kit+ progenitor cells was impaired in the laser?injured diabetic mice compared with the laser?injured control mice. Overall, diabetes did not exert a significant effect on the generation of experimental CrNV. However, diabetes reduced laser?induced ChNV through downregulation of intrachoroidal progenitor cell infiltration and angiogenic factor expression.

SUBMITTER: Liu G

PROVIDER: S-EPMC6172380 | biostudies-other | 2018 Sep

REPOSITORIES: biostudies-other

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Streptozotocin‑induced diabetic mice exhibit reduced experimental choroidal neovascularization but not corneal neovascularization.

Liu Gaoqin G Chen Lei L Cai Qinhua Q Wu Hongya H Chen Zhigang Z Zhang Xueguang X Lu Peirong P

Molecular medicine reports 20180903 5

The present study aimed to investigate the effects of diabetes mellitus (DM) on the generation of experimental corneal neovascularization (CrNV) and choroidal neovascularization (ChNV). Diabetes was induced in mice by intraperitoneal injection of streptozotocin (STZ). Experimental CrNV and ChNV were induced by alkali injury and laser photocoagulation, respectively. CrNV and ChNV were compared between the STZ‑induced diabetic mice and control mice two weeks after injury. Relative expression of an ...[more]

PMID: 30221697

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Project description:BackgroundAdipose-derived mesenchymal stem cells (ASCs) therapy is emerging as a novel therapeutic option for the treatment of a variety of diseases including diabetes and diabetic wound healing. Multiple studies indicate that ASCs could promote wound healing and reverse diabetes. However, whether ASCs from diabetic donors retain their therapeutic functions and the mechanisms of how ASCs contribute to wound healing remain largely unknown. In this study, we explored the cutaneous wound healing ability of ASCs collected from C57BL/6 mice that had been rendered diabetic with streptozotocin (STZ).MethodsASCs were harvested from adipose tissues of type 1 diabetic (T1D) or normal C57BL/6 mice. Cell phenotypes were evaluated by flow cytometry analysis, and cell differentiation into adipocytes, chondrocytes, and osteocytes was compared. Secretions of transforming growth factor β (TGF-β1), basic fibroblast growth factor (bFGF), and vascular endothelial growth factor (VEGF) by ASCs were assessed by ELISA. Migration and proliferation of fibroblasts co-cultured with T1D ASCs or control ASCs were also compared. The therapeutic effects of T1D and control ASCs in promoting wound closure were measured in vivo in a T1D wound mouse model. Granulation tissues were collected and stained with H&E at 14th day. CD34 and collagen I were detected by immunohistochemistry. Expressions of IL-6, α-SMA, CD31, collagen I, and collagen III were quantified by real-time PCR. GFP-expressing ASCs were used to trace in vivo cell differentiation.ResultsT1D ASCs and control ASCs showed similar expression of cell surface markers (CD29, CD34, CD105) and proliferation pattern. They can both differentiate into different cell types. T1D ASCs secreted similar amounts of VEGF and bFGF, but less TGF-β compared with control ASCs. Like control ASCs, T1D ASCs promoted the proliferation and migration of skin fibroblast cells. When injected in cutaneous wound of T1D mice, T1D ASCs increased wound closure and hair follicle regeneration at a comparable extent as ASCs. Mice receiving T1D ASCs or ASCs exhibited significantly higher expressions of collagen I, collagen III, and CD31 and reduced expression of IL-6 in wound tissues. Immunohistochemistry staining showed increased angiogenesis in mice receiving ASCs as was evident by increased CD34+ cells and collagen I staining. GFP+ ASCs injection showed that ASCs differentiated into fibroblasts and endothelial cells in vivo.ConclusionsOur results suggest that T1D ASCs could accelerate cutaneous wound healing. Mechanisms may include increasing fibroblast growth and migration, skin angiogenesis, and differentiation into fibroblasts and endothelial cells. This study provides evidence that diabetic ASCs may be used as a therapeutic option in cutaneous wound healing in diabetic recipients.

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Streptozotocin?induced diabetic mice exhibit reduced experimental choroidal neovascularization but not corneal neovascularization.

Publications

Streptozotocin‑induced diabetic mice exhibit reduced experimental choroidal neovascularization but not corneal neovascularization.

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