22 results about "CD31" patented technology

The invention provides an application of a super enhancer inhibitor JQ-1 in preparation of peripheral artery disease related drugs, relates to the technical field of biomedicine, and discloses a core effect of the super enhancer inhibitor JQ-1 in peripheral artery disease ischemia repair. The traditional Chinese medicine composition can significantly accelerate blood flow recovery of ischemic limbs, up-regulate mRNA and protein expression of a vascular marker CD31 in gastrocnemius muscle tissues, effectively increase vascular density and promote angiogenesis. Aiming at the defects of the existing treatment means in the aspect of ischemic tissue angiogenesis, the application provides a brand new molecular targeted treatment scheme for high-risk groups such as patients with diabetes-related peripheral artery diseases, and can significantly reduce the risk of lower limb amputation and the incidence rate of related cardiovascular adverse events such as coronary heart disease and stroke; the technical blank of specific targeted therapy of peripheral artery diseases is filled, a solid scientific basis and a key direction are provided for research and development of novel drugs, and the specific targeted therapy method has extremely high clinical application value and wide research and development prospects.

This invention discloses a method for preparing and applying a shell-core composite flexible biomaterial. The flexible biomaterial consists of an outer PMMA electrospun layer, a middle PTFF or PE layer, and a core PEG hydrogel; both the PMMA electrospun layer and the middle layer are porous. This flexible material is soft and elastic, exhibiting good film-forming and osteogenic induction effects. Animal experiments have confirmed that, compared to traditional bone cement, the flexible composite bone cement-induced biofilm shows an increase in CD31-positive cells (representing angiogenesis) and M2 macrophages (representing tissue repair), exhibiting better film-forming properties. It is a promising composite biomaterial that can be widely applied in the treatment of soft tissue defects, bone defects, and bone infections, achieving better therapeutic effects.

The invention relates to the technical field of biological medicine and tissue engineering, in particular to a tissue engineering blood vessel and a preparation method and application thereof. The tissue engineering blood vessel is obtained by modifying interleukin 24 (IL-24) on the surface of an acellular blood vessel, after the tissue engineering blood vessel is transplanted into a body, the number of CD31 + and CD34 + cells can be remarkably increased, and infiltration of M2 type macrophages (CD163 +) on the surface of the blood vessel is remarkably increased; the expression of HIF-1 alpha (hypoxia marker) and MMP9 is obviously reduced; the expression of the nerve specific protein S-100 is obviously increased, thrombosis and intimal hyperplasia are effectively inhibited, and the patency rate of transplanted blood vessels is obviously increased.

The invention relates to a method for simultaneously separating and extracting primary cells of pulmonary vascular endothelium and smooth muscle, and belongs to the technical field of cell culture. The method comprises the following steps: S1, digesting lung vascular tissues by using type I collagenase, and filtering to obtain digested cells; s2, incubating the digestive cells with CD31 magnetic beads to obtain magnetic bead incubated cells; s3, uniformly mixing a buffer solution containing fetal calf serum with the magnetic bead incubation cells, standing, and collecting supernate; s4, adding the supernate into an LS sorting column, collecting negative cells, and culturing with an SMCM complete medium to obtain primary cells of pulmonary vascular smooth muscle; and S5, adding an EGM complete medium into the treated LS sorting column, flushing the cells in the LS sorting column into a culture dish coated with rat tail collagen, and culturing to obtain the primary lung vascular endothelial cells. The primary cells obtained by the method are large in quantity, strong in activity and good in adherence effect; other types of cells are less polluted; economic cost is low, and operation is convenient and fast.

The application discloses application of harman alkaline in preparation of a medicine for treating and / or preventing myocardial infarction; the application firstly finds that the harman alkaline can be used for treating and / or preventing myocardial infarction. Meanwhile, the harman alkaline can significantly reduce a myocardial infarction area, improve heart function, and promote blood vessel neogenesis in an infarction edge area; and the harman alkaline can also up-regulate protein expression of CD31. In a cell experiment, the harman alkaline can promote HUVEC cell migration and proliferation after H2O2 injury. The application discloses the anti-myocardial infarction effect of the harman alkaline, provides a new medicine for myocardial infarction treatment, and has important clinical application value.

Inventors have synthesized peptides allowing an engagement of intact CD31 molecules on all the healthy endothelial cells and resting blood platelets and leukocytes that can enter in contact with an implanted device. Those cells can therefore receive the “leave-me-alone” signal delivered by the trans-homophilic engagement of CD31, which is essential to maintain the homeostasis in the circulation and vascularized tissues. Thrombotic or life-threatening occurrence of hemorrhagic or thromboembolic complications have impaired the use of endovascular devices. The devices bearing the mimicking peptides of the present invention are rapidly integrated, because they are perceived by blood platelets and leukocytes as a healthy endothelium, a “self” component. Furthermore, their ability to be rapidly endothelialized with a physiologic endothelial cell phenotype also limits platelet and leukocyte activation at the site of device implantation in the long-term. Accordingly, the present invention relates to peptides mimicking the trans-homophilic CD31-CD31 domain 1 and 2 intercellular interaction.

The invention belongs to the technical field of biology, and particularly relates to separation and application of proteasome-rich human placenta-derived vascular stem cell outer vesicles. The extracellular vesicles provided by the invention are derived from human placenta source blood vessel promoting stem cells, and the human placenta source blood vessel promoting stem cells show that markers PAI-1 are positive, MECOM is positive, CD201 is positive, CD44 is positive, CD73 is positive, HLA-ABC is positive, CD34 is negative, CD31 is negative and CD326 is negative. Compared with human umbilical cord mesenchymal stem cell outer vesicles, the human placenta-derived vascular stem cell outer vesicles provided by the invention are rich in proteasomes and angiogenic protein factors, wherein the proteasomes have high chymotrypsin-like activity. Moreover, in-vivo and in-vitro experimental data show that the human placenta-derived vascular stem cell outer vesicles provided by the invention are rich in proteasomes, and can degrade accumulation of HIF and inhibit cell apoptosis; the medicine has a treatment effect on myocardial infarction.

A noninvasive blood-based biopsy measures surface protein receptors on specific circulating cell populations. Dysregulated quantities of specific surface protein receptors on specific circulating cells indicate the diseased tissue origin. Thus, specific circulating cells serve as proxies for diseased tissue cells as they are shed from such tissues. This approach can be used not only for preeclampsia but also for other vascular disorders where detecting surface protein receptors associated with particular disorders can increase sensitivity and disease specificity. Detection of a high level VEGFR1 on isolated circulating cells that are immunopositive for CD34 and CD31 can be used to identify and treat subjects suffering from preeclampsia.

The invention discloses a primary endocardial endothelial cell extraction method suitable for cardiovascular disease research. Non-specific components are removed through directional sampling, enzyme digestion and mechanical dispersion of an endocardium microscopic spatula and in combination with a CD31 positive selection and CD36 negative selection combined strategy; after culture, Npr3 backtracking, functional verification and passage limitation (less than or equal to P2) are used for controlling quality. According to the method, the cells with the purity of 80-90%, the motility rate of more than or equal to 85% and stable Npr < 3 + > proportion can be obtained, and compared with a traditional method, the method has the advantages in the aspects of material taking specificity, function fidelity and repeatability. The invention provides a reliable cell source for cardiovascular disease research and transformation application.

This invention belongs to the field of biomedical technology, specifically disclosing an injectable embolic agent, its preparation method, and its application. The embolic agent is a hydrocolloid system containing core-shell structured nanoparticles: the core contains Cu... 2+ Salt and ATOX1 inhibitors, where ATOX1 inhibitors can inhibit copper ion efflux and promote intracellular copper accumulation, and interact with Cu 2+ It synergistically induces copper death in tumor cells; the shell is a thermosensitive block copolymer hydrogel that can interact with Cu. 2+ Coordination bonds are formed, enhancing the stability of nanoparticles, while a sol-gel transition occurs at physiological temperatures, enabling precise vascular embolization; the overall core-shell structure allows for the formation of Cu... 2+ The sustained-release effect of ATOX1 inhibitors was observed. In the VX2 rabbit hepatocellular carcinoma model, this embolization agent significantly improved tumor necrosis rate and reduced metastasis rate compared to traditional iodized oil embolization; it also downregulated hypoxia- and angiogenesis-related factors such as HIF-1α, VEGF, and CD31, inhibited MMP9-mediated tumor invasion and metastasis, and promoted CD8+. + T-cell infiltration effectively improves the tumor immunosuppressive microenvironment after transarterial chemoembolization.

The invention relates to a fusion protein for promoting wound repair and application thereof, and belongs to the technical field of biomedicine. The fusion protein is IL-10-bFGF-VEGF165, the amino acid sequence of the fusion protein is shown as SEQ ID NO: 4, and the fusion protein is formed by sequentially connecting an IL-10 functional fragment (SEQ ID NO: 1), a bFGF functional fragment (SEQ ID NO: 2) and a VEGF165 functional fragment (SEQ ID NO: 3) through (Gly4Ser) 3 flexible connecting peptide. The invention also provides a preparation method of the fusion protein, which comprises the steps of recombinant expression vector construction, transformation induced expression, protein purification and the like, and application of the fusion protein in preparation of products for promoting wound repair. Experiments show that the fusion protein can significantly promote proliferation and migration of human skin fibroblasts, up-regulate expression of VEGF and CD31 in mouse wound tissue, enhance local angiogenesis ability and shorten wound healing time, the effect of the fusion protein is superior to that of single bFGF, and a new effective scheme is provided for wound repair.

The invention provides application of an NCOA3 polyQ structural domain as a target spot in preparation of a medicine for relieving lower limb ischemic diseases, relates to the technical field of biomedicine, and aims to solve the problems that in the prior art, blood flow reperfusion recovery of the lower limb ischemic diseases is poor, collateral vessels are insufficient in formation, and safe and effective targeted intervention means are lacked. By constructing a mouse lower limb ischemia model, it is proved that blood flow recovery and collateral angiogenesis after ischemia are remarkably inhibited by Nco3polyQ structural domain deletion: compared with a WT mouse, postoperative blood flow perfusion of an Nco3Q / Q mouse is recovered slowly, and the blood flow of the affected side is only recovered by 60% on the 21st day after the operation; the CD31 positive region of the gastrocnemius muscle tissue on the 14th day after the operation is obviously reduced, and the mRNA expression of the blood vessel marker gene Pecam1 is reduced. On the basis, an intervention strategy aiming at the NCOA3 polyQ structural domain is used for preparing the medicine for relieving the lower limb ischemic disease, and a new treatment strategy and a potential target are provided for the ischemic limb disease.

As used herein, PD-1 + CD38 hi CD8 + Methods are provided for targeting T cells to reduce apoptosis of leukocytes (e.g., lymphocytes). + CD38 hi CD8 + Methods for inducing apoptosis of leukocytes in a subject using adoptive cell therapy with T cells are provided. + CD38 hi CD8 + T cells are dysfunctional and have the ability to kill target cells that express the CD31 receptor, including CD4 and CD8 T cells and endothelial cells.

The application belongs to the field of biological medicine, and provides application of TGF-beta / Smad signal pathway in treatment of corneal neovascularization after corneal alkali burn. The application proves that by inhibiting the TGF-beta / Smad signal pathway, the alkali burn-induced corneal neovascularization can be significantly reduced, and the corneal pathological damage is improved, and the mechanism of action involves regulating M2 type macrophage polarization and inhibiting the process of cellular ferroptosis of corneal tissue. It is found that by using a specific inhibitor SB-431542, the expression of TGF-beta1 and p-Smad2 / 3 proteins can be effectively reduced, the angiogenic factors such as VEGFA and CD31 are reduced, the inflammatory factors such as IL-4 and IL-10 are down-regulated, the GSH level is restored, and the Fe 2+ and MDA contents are reduced. The application is suitable for developing a targeted therapeutic drug for pathological neovascularization after corneal alkali burn, and provides a theoretical basis.

The present invention relates to a culture method for culturing a population of endothelial colony-forming cells (ECFC) derived from umbilical cord blood, the method comprising: (a) holding an umbilical cord blood sample obtained from a subject at a temperature of 4 DEG C to 15 DEG C for 24 hours to 72 hours; (b) isolating mononuclear cells from the blood sample; (c) inoculating the mononuclear cells on a culture substrate; (d) culturing the inoculated adherent monocytes in a culture medium for about 5 days to about 21 days to form colonies comprising cells; and (e) culturing the cells which express the CD31, the CD34, the CD105, the CD144, the CD146, the CD157 and the VEGFR2 (vascular endothelial growth factor receptor 2) but do not express the CD45, the CD14 and the CD90.

The invention discloses application of avenanthramide D in preparation of a medicine for inhibiting angiogenesis, and relates to the technical field of biological medicine. Avenanthramide D is applied to intervene HUVEC cells, cell viability, cell apoptosis rate and angiogenesis ability after intervention are detected, and it is found that avenanthramide D can inhibit HUVEC cell proliferation, promote HUVEC cell apoptosis and inhibit HUVEC cell angiogenesis. A further experiment shows that the avenanthramide D reduces the integrity of an endothelial barrier by reducing the protein expression of a vascular endothelial growth factor A (VEGFA) and a platelet endothelial cell adhesion molecule 1 (CD31) in HUVEC cells, so that angiogenesis is blocked.

The invention provides application of an NCOA3 polyQ structural domain in preparation of a medicine for relieving ocular vascular abnormal hyperplasia diseases, relates to the technical field of biomedicine, and aims to solve the problems that in the prior art, an ocular pathological angiogenesis mechanism is complex, and safe and effective targeted intervention means are lacked. The construction of a mouse corneal micropocket pathological angiogenesis model proves that Nco3polyQ structural domain deletion can significantly inhibit corneal neovascularization: compared with a WT mouse, the Nco3wt / Q mouse corneal tissue CD31 positive signal is reduced, the number of corneal neovascularization in the Nco3Q / Q mouse is minimum, and the CD31 positive area is minimum; meanwhile, qPCR (quantitative polymerase chain reaction) detection of corneal tissues shows that mRNA (messenger ribonucleic acid) expression of the vascular marker genes Pecam1 and Cdh5 is in a decreasing trend and is further decreased in an Nco3Q / Q mouse. On the basis, the intervention strategy aiming at the NCOA3 polyQ structural domain is used for preparing the medicine for relieving the abnormal hyperplasia diseases of the ocular blood vessels, and a new treatment strategy and a potential target are provided for related diseases of the ophthalmology department.

The invention relates to a marker for auxiliary diagnosis or identification of vascular cognitive impairment, a kit and application. In particular to a marker combination for diagnosis, auxiliary diagnosis or identification of vascular cognitive impairment. The marker combination comprises small extracellular vesicles carrying CD31 expression. The marker combination provided by the invention has the advantages of high specificity and good sensitivity, and can be used for diagnosis, auxiliary diagnosis or identification of vascular cognitive impairment.

The invention provides identification and application of a left heart disease-related pulmonary arterial hypertension pulmonary artery part endothelial mesenchymal transformation subgroup, and finds that according to the ratio of expression levels of endothelial cell markers (such as VWF and CD31) and mesenchymal cell markers (such as alpha-SMA, DCN and TAGLN) in an EndMT cell subgroup, the expression level of the endothelial cell markers (such as VWF and CD31) in the EndMT cell subgroup is determined, and the expression level of the mesenchymal cell markers (such as alpha-SMA, DCN and TAGLN) in the EndMT cell subgroup is determined. And the expression levels of TGF-beta1, TNFRSF1A, CXCL12, CCL14, CD74, TGFBR2 and CD44 in the EndMT cell subset can (i) be used for typing patients of PH-LHD according to different periods of mesenchymal transformation of endothelial cells; and / or (ii) is used for judging whether a patient suffering from the left heart disease related pulmonary hypertension (PH-LHD) is suitable for adopting a CD74 inhibitor, and / or a CD44 inhibitor is used as a target spot for treating the left heart disease related pulmonary hypertension (PH-LHD).

The present application relates to a marker, a kit and a use for assisting in diagnosing or differentiating a vascular cognitive impairment. Specifically, the present application relates to a marker combination for diagnosing, assisting in diagnosing or differentiating a vascular cognitive impairment, wherein the marker combination comprises small extracellular vesicles carrying CD31 expression. The present application provides the marker combination with the advantages of high specificity and good sensitivity, and the marker combination can be used for diagnosing, assisting in diagnosing or differentiating a vascular cognitive impairment.

The present application relates to biomedical functional materials and nano drug delivery technology, and particularly relates to a double-response nano hydrogel for promoting chronic wound healing of diabetes, a preparation method and application. The hydrogel is stable in delivery of miR-144-5p by constructing chitosan / sodium tripolyphosphate / hyaluronic acid nanoparticles, and is synergistically loaded with oxymatrine in a gelatin-TG enzyme crosslinking hydrogel matrix, so that in-situ gelation and sequential release of double functional drugs are realized under body temperature. Animal experiments prove that the composition can significantly accelerate wound closure, improve VEGF and CD31 expression and reconstruct dermal vascular network, and has good biocompatibility and controlled release performance, and has a wide clinical application prospect.

The invention discloses application of beta-alanine in angiogenesis resistance, and relates to the technical field of biological medicines. The invention provides an application of beta-alanine in preparation of an anti-angiogenesis medicine. The beta-alanine provided by the invention effectively inhibits the expression and secretion of ANG (Angiogenic Growth Growth Factor) and VEGF (vascular endothelial growth factor). The beta-alanine can directly inhibit proliferation and tubulation of vascular endothelial cells in a tumor-independent form. Tumor formation experiments are carried out in nude mice, the treatment of the beta-alanine reduces the volume of tumors, effectively inhibits the expression of hypoxia-inducible factors HIF1-alpha, ANG and VEGF, and the treatment of the beta-alanine significantly reduces the number of CD31 + and Ki67 + endothelial cells and the expression of CD31. The beta-alanine shows good anti-angiogenesis activity, can inhibit angiogenesis in a multi-target manner, and is an effective anti-angiogenesis drug for treating diseases, especially for treating tumors.