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Bone marrow MiR-181a/b-CXCR4 signaling axis impairs hematopoiesis, monocytosis, and angiogenesis in diabetic critical limb ischemia

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE196566 | GEO | 2023/10/01

REPOSITORIES: GEO

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Bone marrow MiR-181a/b-CXCR4 signaling axis impairs hematopoiesis, monocytosis, and angiogenesis in diabetic critical limb ischemia [BM_CHOW]

Project description:We report transcriptomic changes in bone marrow cells of systemic miR-181a2b2 KO mice in response after chow diet feeding and hindlimb ischemia

2023-10-01 | GSE196562 | GEO

Bone marrow MiR-181a/b-CXCR4 signaling axis impairs hematopoiesis, monocytosis, and angiogenesis in diabetic critical limb ischemia [BM_HFSC]

Project description:We report transcriptomic changes in bone marrow cells of systemic miR-181a2b2 KO mice in response after HFSC diet feeding and hindlimb ischemia

2023-10-01 | GSE196561 | GEO

Bone marrow MiR-181a/b-CXCR4 signaling axis impairs hematopoiesis, monocytosis, and angiogenesis in diabetic critical limb ischemia [SM_CHOW_HFSC]

Project description:We report transcriptomic changes in skeletal muscle of systemic miR-181a2b2 KO mice in response to chow and HFSC diet feeding and hindlimb ischemia

2023-10-01 | GSE196565 | GEO

Therapeutic angiogenesis in critical limb ischemia.

Project description:Critical limb ischemia (CLI) is a severe form of peripheral artery disease associated with high morbidity and mortality. The primary therapeutic goals in treating CLI are to reduce the risk of adverse cardiovascular events, relieve ischemic pain, heal ulcers, prevent major amputation, and improve quality of life (QoL) and survival. These goals may be achieved by medical therapy, endovascular intervention, open surgery, or amputation and require a multidisciplinary approach including pain management, wound care, risk factors reduction, and treatment of comorbidities. No-option patients are potential candidates for the novel angiogenic therapies. The application of genetic, molecular, and cellular-based modalities, the so-called therapeutic angiogenesis, in the treatment of arterial obstructive diseases has not shown consistent efficacy. This article summarizes the current status related to the management of patients with CLI and discusses the current findings of the emerging modalities for therapeutic angiogenesis.

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MicroRNA-375 repression of Kruppel-like Factor 5 Improves Angiogenesis in Diabetic Critical Limb Ischemia

Project description:Screening of dysregulated microRNAs identified miR-375 as a potential biomarker and therapeutic target which may improve outcomes in diabetic critical limb ischemia.

2022-08-10 | GSE210778 | GEO

Myocyte specific overexpression of myoglobin impairs angiogenesis after hind-limb ischemia.

Project description:In preclinical models of peripheral arterial disease the angiogenic response is typically robust, though it can be impaired in conditions such as hypercholesterolemia and diabetes where the endothelium is dysfunctional. Myoglobin (Mb) is expressed exclusively in striated muscle cells. We hypothesized that myocyte specific overexpression of myoglobin attenuates ischemia-induced angiogenesis even in the presence of normal endothelium.Mb overexpressing transgenic (MbTg, n=59) and wild-type (WT, n=56) C57Bl/6 mice underwent unilateral femoral artery ligation/excision. Perfusion recovery was monitored using Laser Doppler. Ischemia-induced changes in muscle were assessed by protein and immunohistochemistry assays. Nitrite/nitrate and protein-bound NO, and vasoreactivity was measured. Vasoreactivity was similar between MbTg and WT. In ischemic muscle, at d14 postligation, MbTg increased VEGF-A, and activated eNOS the same as WT mice but nitrate/nitrite were reduced whereas protein-bound NO was higher. MbTg had attenuated perfusion recovery at d21 (0.37+/-0.03 versus 0.47+/-0.02, P<0.05), d28 (0.40+/-0.03 versus 0.50+/-0.04, P<0.05), greater limb necrosis (65.2% versus 15%, P<0.001), a lower capillary density, and greater apoptosis versus WT.Increased Mb expression in myocytes attenuates angiogenesis after hind-limb ischemia by binding NO and reducing its bioavailability. Myoglobin can modulate the angiogenic response to ischemia even in the setting of normal endothelium.

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Impaired angiogenesis in diabetic critical limb ischemia is mediated by a miR-130b-INHBA signaling axis

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-05-22 | GSE204706 | GEO

Danhong Promotes Angiogenesis in Diabetic Mice after Critical Limb Ischemia by Activation of CSE-H 2 S-VEGF Axis.

Project description:The aim of this paper is to investigate effect and mechanism of Danhong injection (DH) on angiogenesis in the diabetic hind limb ischemia mouse model. Thirty diabetic hind limb ischemic model mice and ten normal mice, established by intraperitoneal (i.p.) injection of streptozotocin (STZ) or PBS and ligation/excision of femoral artery, and then twenty diabetic hind limb ischemic model mice of all were evenly randomized to saline (control, n = 10) and DH i.p. injection (2?mL/kg weight for 7 days, n = 10) groups. Limb perfusion recovery and femoral blood hydrogen sulfide (H2S) and vessel regeneration and lower limb vascular endothelial growth factor (VEGF)/cystathionine ?-lyase (CSE) expression were evaluated during intervention and after euthanasia, respectively. DH i.p. increased ischemic limb perfusion and promoted collateral circulation generation without decreasing blood glucose level. Increased local CSE-H2S-VEGF expression contributed to beneficial effects of DH injection. In conclusion, activation of local CSE-H2S-VEGF axis might participate in proangiogenesis effects of DH injection in diabetic hind limb ischemia model mice, suggesting a potential therapy for diabetic patients with critical limb ischemia.

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Bmal1 Downregulation Worsens Critical Limb Ischemia by Promoting Inflammation and Impairing Angiogenesis.

Project description:Critical limb ischemia (CLI) is the most advanced clinical stage of peripheral vascular disease with high mobility and mortality. CLI patients suffer from lower extremity rest pain, ulceration, and gangrene caused by insufficient blood and oxygen supply. Seeking for effective biomarkers and therapeutic targets is of great significance for improving the life quality of CLI patients. The circadian clock has been reported to be involved in the progression of kinds of cardiovascular diseases. Whether and how circadian genes play a role in CLI remains unknown. In this study, by collecting femoral artery and muscle specimens of CLI patients who underwent amputation, we confirmed that the circadian gene Bmal1 is downregulated in the CLI femoral artery and ischemic distal lower limb muscle. Furthermore, we verified that Bmal1 affects CLI by regulating lipid metabolism, inflammation, and angiogenesis. A hindlimb ischemia model performed in wild-type and Bmal1-/- mice confirmed that Bmal1 disruption would lead to impaired angiogenesis. In vitro experiments indicated that the decreased expression of Bmal1 would increase ox-LDL uptake and impair endothelial cell functions, including proliferation, migration, and tube formation. As for mechanisms, Bmal1 represses inflammation by inhibiting lipid uptake and by activating IL-10 transcription and promotes angiogenesis by transcriptionally regulating VEGF expression. In conclusion, we provide evidence that the circadian gene Bmal1 plays an important role in CLI by inhibiting inflammation and promoting angiogenesis. Thus, Bmal1 may be an effective biomarker and a potential therapeutic target in CLI.

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Impaired angiogenesis in diabetic critical limb ischemia is mediated by a miR-130b-INHBA signaling axis [ischemic gastrocnemius]

Project description:We report transcriptomic changes in the EC fraction of the gastrocnemius muscle after intramuscular injection of negative control mimic and miR-130b mimic.

2023-05-21 | GSE202856 | GEO

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