Thromboxane A<sub>2</sub>induces blood flow recovery via platelet adhesion to ischaemic regions

Aoki, Hideki; Yoshiya, Ikuto; Eshima, Koji; Kato, Shintaro; Ogawa, Fumihiro; Hosono, Kanako; Oba, Kazuhito; Tamaki, Hideaki; Sakagami, Hiroyuki; Shibuya, Masabumi; Narumiya, Shuh; Murakami, Masataka

doi:10.1093/cvr/cvv139

Cited by 29 publications

(35 citation statements)

References 45 publications

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“…Furthermore, using in vivo microscopy, we showed that platelet adhesion to microvessels in the ischemic muscle was suppressed by P-selectin antibody treatment in WT but not in TP À/À . 32 In the present study, we showed the plasma levels of VEGF and SDF1 were increased by C57-mTXAS treatment in WT. Although not definitively, these results suggested that the TXASeTXA 2 eTP receptor axis induced platelet activation and released angiogenesis stimulating factors.…”

Section: Discussionsupporting

confidence: 58%

“…35,36 We showed that TP signalingenhanced PSGL-1 expression on ECs under hypoxic condition that resulted in heterogeneous angiogenicity of the ECs. 32 Present study showed that the expression of PSGL-1 on ECs was enhanced by C57-mTXAS treatment in WT but not in TP À/À (Fig. 5).…”

Section: Discussionmentioning

confidence: 52%

“…Our previous study showed that the expression of P-selectin on platelets was enhanced after surgical treatment in WT but not in TP À/À . 32 In the present study, we estimated the expression of P-selectin on the platelet surface in peripheral blood and showed that the population of P-selectin þ CD41 þ platelets was enhanced in C57-mTXAS-treated WT mice compared with C57-EV-treated WT mice (Fig. 4A).…”

Section: Discussionmentioning

confidence: 56%

“…Although we did not estimate the population of P-selectin þ CD41 þ platelets in TP À/À after these two vector treatments, we expected there was no significant difference in the expression of P-selectin on the platelets based on our previous studies. 17,20,32,33 As reported in the introduction, platelets contain proangiogenic stimulating factors, VEGF, SDF-1, FGF-2, and PDGF that were secreted by activated platelets. [3][4][5] Platelet-derived proangiogenic stimulating factors induce angiogenesis and tumor metastasis formation.…”

Section: Discussionmentioning

confidence: 96%

“…Our previous study suggested that mobilization of BM-derived CXCR4 þ VEGFR1 þ -induced angiogenesis and tumor metastasis formation. 32,33 VEGF and SDF-1 are known to induce mobilization of BM-derived VEGFR1 þ cells. 16 In addition, VEGF and SDF-1 released from platelets promote tumor metastasis and angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

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Thromboxane A synthase enhances blood flow recovery from hindlimb ischemia

Aoki

Nakamura

Yoshiya

et al. 2016

Journal of Surgical Research

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Section: Discussionsupporting

confidence: 58%

Section: Discussionmentioning

confidence: 52%

Section: Discussionmentioning

confidence: 56%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

See 3 more Smart Citations

Thromboxane A synthase enhances blood flow recovery from hindlimb ischemia

Aoki

Nakamura

Yoshiya

et al. 2016

Journal of Surgical Research

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Thromboxane prostanoid signaling in macrophages attenuates lymphedema and facilitates lymphangiogenesis in mice

et al. 2023

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Background Accumulating evidence suggests that prostaglandin E2, an arachidonic acid (AA) metabolite, enhances lymphangiogenesis in response to inflammation. However, thromboxane A2 (TXA2), another AA metabolite, is not well known. Thus, this study aimed to determine the role of thromboxane prostanoid (TP) signaling in lymphangiogenesis in secondary lymphedema. Methods and results Lymphedema was induced by the ablation of lymphatic vessels in mouse tails. Compared with wild-type mice, tail lymphedema in Tp-deficient mice was enhanced, which was associated with suppressed lymphangiogenesis as indicated by decreased lymphatic vessel area and pro-lymphangiogenesis-stimulating factors. Numerous macrophages were found in the tail tissues of Tp-deficient mice. Furthermore, the deletion of TP in macrophages increased tail edema and decreased lymphangiogenesis and pro-lymphangiogenic cytokines, which was accompanied by increased numbers of macrophages and gene expression related to a pro-inflammatory macrophage phenotype in tail tissues. In vivo microscopic studies revealed fluorescent dye leakage in the lymphatic vessels in the wounded tissues. Conclusions The results suggest that TP signaling in macrophages promotes lymphangiogenesis and prevents tail lymphedema. TP signaling may be a therapeutic target for improving lymphedema-related symptoms by enhancing lymphangiogenesis.

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Vascular endothelial growth factor receptor 1 (VEGFR1) tyrosine kinase signaling facilitates granulation tissue formation with recruitment of VEGFR1+ cells from bone marrow

et al. 2017

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Vascular endothelial growth factor (VEGF)-A facilitates wound healing. VEGF-A binds to VEGF receptor 1 (VEGFR1) and VEGFR2 and induces wound healing through the receptor's tyrosine kinase (TK) domain. During blood flow recovery and lung regeneration, expression of VEGFR1 is elevated. However, the precise mechanism of wound healing, especially granulation formation on VEGFR1, is not well understood. We hypothesized that VEGFR1-TK signaling induces wound healing by promoting granulation tissue formation. A surgical sponge implantation model was made by implanting a sponge disk into dorsal subcutaneous tissue of mice. Granulation formation was estimated from the weight of the sponge and the granulation area from the immunohistochemical analysis of collagen I. The expression of fibroblast markers was estimated from the expression of transforming growth factor-beta (TGF-β) and cellular fibroblast growth factor-2 (FGF-2) using real-time PCR (polymerase chain reaction) and from the immunohistochemical analysis of S100A4. VEGFR1 TK knockout (TK) mice exhibited suppressed granulation tissue formation compared to that in wild-type (WT) mice. Expression of FGF-2, TGF-β, and VEGF-A was significantly suppressed in VEGFR1 TK mice, and the accumulation of VEGFR1 cells in granulation tissue was reduced in VEGFR1 TK mice compared to that in WT mice. The numbers of VEGFR1 cells and S100A4 cells derived from bone marrow (BM) were higher in WT mice transplanted with green fluorescent protein (GFP) transgenic WT BM than in VEGFR1 TK mice transplanted with GFP transgenic VEGFR1 TK BM. These results indicated that VEGFR1-TK signaling induced the accumulation of BM-derived VEGFR1 cells expressing F4/80 and S100A4 and contributed to granulation formation around the surgically implanted sponge area in a mouse model.

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Thromboxane A₂induces blood flow recovery via platelet adhesion to ischaemic regions

Abstract: These results indicated that TP signalling facilitates ischaemia-induced angiogenesis via P-selectin-mediated platelet adhesion to PSGL-1 on the ECs at ischaemic sites and the supply of pro-angiogenic factors by the adherent platelets.

Cited by 29 publications

References 45 publications

Thromboxane A synthase enhances blood flow recovery from hindlimb ischemia

Thromboxane A synthase enhances blood flow recovery from hindlimb ischemia

Thromboxane prostanoid signaling in macrophages attenuates lymphedema and facilitates lymphangiogenesis in mice

Vascular endothelial growth factor receptor 1 (VEGFR1) tyrosine kinase signaling facilitates granulation tissue formation with recruitment of VEGFR1+ cells from bone marrow

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Thromboxane A2induces blood flow recovery via platelet adhesion to ischaemic regions

Abstract: These results indicated that TP signalling facilitates ischaemia-induced angiogenesis via P-selectin-mediated platelet adhesion to PSGL-1 on the ECs at ischaemic sites and the supply of pro-angiogenic factors by the adherent platelets.

Cited by 29 publications

References 45 publications

Thromboxane A synthase enhances blood flow recovery from hindlimb ischemia

Thromboxane A synthase enhances blood flow recovery from hindlimb ischemia

Thromboxane prostanoid signaling in macrophages attenuates lymphedema and facilitates lymphangiogenesis in mice

Vascular endothelial growth factor receptor 1 (VEGFR1) tyrosine kinase signaling facilitates granulation tissue formation with recruitment of VEGFR1+ cells from bone marrow

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Thromboxane A₂induces blood flow recovery via platelet adhesion to ischaemic regions