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A matrix metalloproteinase-responsive hydrogel system controls angiogenic peptide release for repair of cerebral ischemia/reperfusion injury

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Neural Regeneration Research 2025年第2期20卷 503-517页

作者： Qi Liu Jianye Xie Runxue Zhou Jin Deng Weihong Nie Shuwei Sun Haiping Wang Chunying Shi Department of Human Anatomy Histology and EmbryologySchool of Basic MedicineQingdao UniversityQingdaoShandong ProvinceChina Department of Neurology The Affiliated Hospital of Qingdao UniversityQingdaoShandong ProvinceChina Department of General Practice The Affiliated Hospital of Qingdao UniversityQingdaoShandong ProvinceChina

Vascular endothelial growth factor and its mimic peptide KLTWQELYQLKYKGI(QK)are widely used as the most potent angiogenic factors for the treatment of multiple ischemic diseases.However,conventional topical drug delivery often results in a burst release of the drug,leading to transient retention(inefficacy)and undesirable diffusion(toxicity)in vivo.Therefore,a drug delivery system that responds to changes in the microenvironment of tissue regeneration and controls vascular endothelial growth factor release is crucial to improve the treatment of ischemic stroke.matrix metalloproteinase-2(MMP-2)is gradually upregulated after cerebral ischemia.Herein,vascular endothelial growth factor mimic peptide QK was self-assembled with MMP-2-cleaved peptide PLGLAG(TIMP)and customizable peptide amphiphilic(PA)molecules to construct nanofiber hydrogel PA-TIMP-QK.PA-TIMP-QK was found to control the delivery of QK by MMP-2 upregulation after cerebral ischemia/reperfusion and had a similar biological activity with vascular endothelial growth factor in vitro.The results indicated that PA-TIMP-QK promoted neuronal survival,restored local blood circulation,reduced blood-brain barrier permeability,and restored motor function.These findings suggest that the self-assembling nanofiber hydrogel PA-TIMP-QK may provide an intelligent drug delivery system that responds to the microenvironment and promotes regeneration and repair after cerebral ischemia/reperfusion injury.

关键词： angiogenesis biomaterial blood-brain barrier cerebral ischemia/reperfusion injury control release drug delivery inflammation QK peptides matrix metalloproteinase-2 neuroprotection self-assembling nanofiber hydrogel

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Regulation of matrix metalloproteinase-2 and matrix metalloproteinase-9 in Abdominal Aortic Aneurysm

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Cardiology Discovery 2023年第3期3卷 212-220页

作者： Shuo Wang Dan Liu Xiaolin Zhang Xiaoxiang Tian Department of Cardiology and Cardiovascular Research Institute General Hospital of Northern Theater CommandShenyang 110016China Department of Cardiology Shengjing Hospital of China Medical UniversityShenyang 110022China.

Abdominal aortic aneurysm (AAA) is a degenerative disease characterized by destruction and progressive expansion of the abdominal aortic wall. An AAA is typically defined as an enlargement of the abdominal aorta with diameter ≥3 cm or ≥50% greater than the suprarenal diameter. The pathological changes associated with AAA include inflammatory cell infiltration, extracellular matrix (ECM) destruction and remodeling, and vascular smooth muscle cell loss. The matrix metalloproteinase (MMP) family of proteins plays an important role in initiation and progression of AAA. Since understanding the regulation of MMP-2 and MMP-9 in AAA is essential for treatment of AAA, this review summarized the regulatory mechanisms of MMPs to provide a reference for exploring novel therapeutic approaches.

关键词： Aortic aneurysm abdominal aortic matrix metalloproteinase-2 matrix metalloproteinase-9

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Distribution and relative activity of matrix metalloproteinase-2 in human coronal dentin

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International Journal of Oral Science 2011年第4期3卷 192-199页

作者： Lee W. Boushell Masaru Kaku Yoshiyuki Mochida Mitsuo Yamauchi Department of Operative Dentistry School of Dentistry University of North Carolina Department of Bio-Prosthodontics Medical and Dental Science Niigata University Graduate School Chuo-ku Department of Periodontology and Oral Biology Division of Oral Biology Boston University Henry M. Goldman School of Dental Medicine Center for Advanced Biomedical Research Dental Research Center School of Dentistry University of North Carolina

The presence of matrix metalloproteinase-2 （MMP-2） in dentin has been reported, but its distribution and activity level in mature human coronal dentin are not well understood. The purpose of this study was to determine the MMP-2 distribution and relative activity in demineralized dentin. Crowns of twenty eight human molars were sectioned into inner （ID）, middle （MD）, and outer dentin （OD） regions and demineralized. MMP-2 was extracted with 0.33 mol·L-1 EDTA/2 mol·L-1 guanidine-HCl, pH 7.4, and MMP-2 concentration was estimated with enzyme-linked immunoabsorbant assay （ELISA）. Further characterization was accomplished by Western blotting analysis and gelatin zymography. The mean concentrations of MMP-2 per mg dentin protein in the dentin regions were significantly different （P=0.043）： 0.9 ng （ID）, 0.4 ng （MD）, and 2.2 ng （OD）, respectively. The pattern of MMP-2 concentration was OD〉ID〉MD. Western blotting analysis detected -66 and -72 kDa immunopositive proteins corresponding to pro- and mature MMP-2, respectively, in the ID and MD, and a -66 kDa protein in the OD. Gelatinolytic activity consistent with MMP-2 was detected in all regions. Interestingly, the pattern of levels of Western blot immunodetection and gelatinolytic activity was MD〉ID〉OD. The eoneentration of MMP-2 in human coronal dentin was highest in the region of dentin that contains the dentinoenamel junction and least in the middle region of dentin. However, levels of Western blot immunodetection and gelatinolytic activity did not correlate with the estimated regional concentrations of MMP-2, potentially indicating region specific protein interactions.

关键词： matrix metalloproteinase-2 human coronal dentin distribution gelatinolytic activity

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Effects of benazepril on renal function and kidney expression of matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-2 in diabetic rats

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Chinese Medical Journal 2006年第10期119卷 814-821页

作者： SUN Shu-zhen WANG Yi LI Qian TIAN Yong-jie LIU Ming-hua YU Yong-hui Department of Pediatrics Shandong Provincial Hospital ShandongUniversity Jinan 250021 China

Background Excessive deposition of extraceUular matrix （ECM） in the kidney is the hallmark of diabetic nephropathy. Increased matrix synthesis has been well documented but the effects of diabetes on degradative pathways, particularly in the in vivo setting. The renal protective effect of these pathways on matrix accumulation has not been fully elucidated. The present study was understaken to investigate the activity of matrix metalloproteinase-2 （MMP-2）, the expression of MMP-2 and tissue inhibitor of metalloproteinase-2 （TIMP-2） in kidney tissues of diabetic rats, and to explore the degradative pathway of type Ⅳ collagen （Ⅳ-C） and the renal protective effects of ACE inhibition- benazepril.

关键词： angiotensin converting enzyme inhibitors diabetic nephropathy renal function matrix metalloproteinase-2 tissue inhibitor of metalloproteinase-2

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Atorvastatin reduces myocardial fibrosis in a rat model with post- myocardial infarction heart failure by increasing the matrix metaHoproteinase-2/tissue matrix metalloproteinase inhibitor-2 ratio

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Chinese Medical Journal 2013年第11期126卷 2149-2156页

作者： AN Zhe YANG Guang HE Yu-quan DONG Ning GE Li-li LI Shu-mei ZHANG Wen-qi Department of Cardiology the Second Hospital Jilin UniversityChangchun Jilin 130041 China Department of Molecular Biology Medical College of NormanB ethune Jilin University Changchun Jilin 130021 China Department of Cardiology China-Japan Union Hospital JilinUniversity Changchun Jilin 130033 China Department of Emergency the First Hospital of Jilin UniversityChangchun Jilin 130021 China

Background The cholesterol-lowering statin drugs have some non-lipid-lowering effects, such as inhibiting myocardial remodeling. However, the underlying mechanism is still unclear. Methods The left anterior descending coronary artery was ligated to establish a rat model of heart failure, and the rats were divided into a sham operation （SO） group, myocardial infarction model （MI） group, and MI-atorvastatin group. Changes in hemodynamic parameters were recorded after the final drug administration. Histological diagnosis was made by reviewing hematoxylin and eosin （HE） stained tissue. Real-time quantitative polymerase chain reaction （PCR） was performed to determine the expressions of type I and type III collagen, matrix metalloproteinase-2 （MMP-2）, and tissue matrix metalloproteinase inhibitor-2 （TIMP-2）. Further, primary rat cardiac fibroblasts were cultured and the MTT assay was performed to determine the effect of atorvastatin on cardiac fibroblast proliferation. Results The model of heart failure was established and the results of HE staining and Masson＇s trichrome staining revealed that the rats in the heart failure group showed obvious hyperplasia of fibrotic tissue, which was significantly reduced in the atorvastatin group. Real-time quantitative PCR showed that the MI group showed a significantly increased expression of type I and type III coltagen, MMP-2, and TIMP-2, but a significantly reduced MMP-2/T＇IMP- 2 ratio. Compared with the MI group, the atorvastatin group showed significantly reduced expression of type I and III collagen, unchanged expression of MMP-2, significantly reduced expression of TIMP-2, and an increased MMP-2/ TIMP-2 ratio. We further found that atorvastatin significantly inhibited the Ang II-induced fibroblast proliferation and the expression of type I and type III collagen in cardiac fibroblasts while increasing the MMP-2/TIMP-2 ratio. Conclusions These data suggest that atorvastatin can inhibit cardiac fibroblast proliferation and enhance collagen degradation by increasing the MMP-2/T

关键词： atorvastatin cardiac fibroblasts matrix metalloproteinase-2 tissue matrix metalloproteinase inhibitor-2

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Effects of irbesartan on the expression of matrix metalloproteinase-2/ tissue inhibitor of metalloproteinase-2 in streptozotocin-induced diabetic rat kidney

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Chinese Medical Journal 2005年第12期118卷 1040-1044页

作者： LIUBi-cheng XUYan MAKun-ling HUANGHai-quan YINLian-fang LIUDian-ge InstituteofNephrology ZhongdaHospitalSoutheastUniversitySchoolofMedicineNanjing210009China

Glomerular hypertrophy and progressive expansion of extracelluar matrix (ECM) have been regarded as the early feature of diabetic nephropathy (DN), which leads to accumulation of ECM and thickening of glomerular basement membrane, and subsequently induces renal fibrosis. Both increasing synthesis and decreasing degradation of matrix components are responsible for matrix accumulation. The later may play more important role in DN that involves a number of matrix metalloproteinases (MMPs). MMPs are a family of proteolytic enzymes whose activity is tightly regulated by tissue inhibitor of metalloproteinases (TIMPs), and the MMP/TIMP ratio is critical for coordinating matrix production and degradation. 1 Recently, considerable evidence suggests that the intrarenal renin-angiotensin system plays an important role in the development of DN. 2 Blockade of the renin-angiotensin system (RAS) by angiotensin-coverting enzyme inhibitor (ACEI) or angiotensin Ⅱ receptor antagonist (AIIRA) delays the progression of renal injury associated with diabetes. 3 AIIRA has been regarded as the first line choice for DN therapy. However, the potential mechanism for AIIRA in the ECM degradative pathway has not been fully elucidated. The present study is to investigate the effect of Irbesartan (Irb), a newly developed AIIRA, on renal expression of MMP-2 and TIMP-2 in streptozotocin (STZ)-induced diabetic rats.

关键词： irbesartan diabetic nephropathy matrix metalloproteinase-2 tissue inhibitor of metalloproteinase-2

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Regulation of mouse blastocyst adhesion,outgrowth and matrix metalloproteinase-2 by focal adhesion kinase

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Chinese Science Bulletin 2003年第5期48卷 475-479页

作者： TIE Guodong TIAN Yongqiang CHEN Shuyi CAO Yujing LIU Zelong DUAN Enkui ZHAO Xingxu State Key Lab of Reproductive Biology Institute of ZoologyChinese Academy of SciencesBeijing 100080China Department of Veterinary Medicine Gansu Agricultural UniversityLanzhou 730070China

The interaction of extracellular matrix-integrin markedly influences the adhesion, outgrowth, differentiation and expression of serine proteinases by the blastocyst, so it is regarded as a vital factor in blastocyst implantation. Al- though the mechanism of extracellular interactions between extracellular matrix and integrins has been well elucidated, the roles of the signaling molecules in the extracellular ma- trix-integrin signal transduction pathway in blastocyst im- plantation are unknown. This limits the understanding of blastocyst implantation and ECM-integrin signal transduc- tion pathway. In the present study, in vitro blastocyst culture and indirect immunocytochemistry, matrix metallopro- teinases (MMPs) zymography and antisense oligodeoxynu- cleotide (ODN) were used to investigate the expression of a fundamental molecule of integrin-dependent signal trans- duction pathways, focal adhesion kinase (FAK), in mouse blastocysts and its influence on mouse blastocyst adhesion, outgrowth and MMP-2. The results showed that mouse blas- tocysts expressed FAK. FAK protein was clustered in the peripheral migrating trophoblast cells and dispersed in the central area of blastocyst outgrowth. Fibronectin triggered pro-MMP-2 and 64 kD MMP-2 activities. The antisense ODN to FAK attenuated pro-MMP-2 and 64 kD MMP-2 activities which decreased abruptly and tended to disappear with increasing concentrations of the antisense ODN. Both mouse blastocyst adhesion and outgrowth on fibronectin were also influenced by the antisense ODN. Up to 20 mg/mL of the antisense ODN concentration, the adhesion and out- growth rates were decreased in a dose-dependent manner. The results indicated that FAK influenced mouse blastocyst adhesion, outgrowth and MMP-2 activity by intracellular signal transduction. In other words, FAK regulates mouse implantation in terms of blastocyst adhesive and invasive abilities.

关键词： focal adhesion kinase matrix metalloproteinase-2 blas-tocyst implantation

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Correlation of RECK with matrix metalloproteinase-2 in Regulation of Trophoblast Invasion of Early Pregnancy

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2006年第6期26卷 738-740页

作者：郭君红邹丽 Department of Obstetrics and Gynecology Union Hospital Tongji Medical College Huazhong University of Science and Technology

To study the role of the reversion-inducing-cysteine-rich protein with Kazal motifs （RECK） gene and matrix metalloproteinase-2 （MMP-2） in the regulation of trophoblast invasion of early pregnancy. Immunohistochemistry, Western blot and gelatin zymography were used to detect the RECK protein expression localization, expression level and MMP-2 activation level in the placental tissues harvested from 52 normal pregnant women （27 in the early pregnancy, 25 in the term pregnancy）. Immunohistochemistry showed that RECK expression was found both in villous tissues of early pregnancy group and term pregnancy group and was mainly observed in cell membrane and cytoplasm of cytotrophoblasts and syneytiotrophoblasts. RECK expression increased with gestational time. RECK expression of early pregnancy group was significantly lower than that of term pregnancy group （P〈0.05）. RECK expression was significantly lower in cellular column （CC） with invasion ability. Western blot showed that the RECK protein expression in early pregnancy group was significantly lower than that in term pregnancy （P〈0.05）. The optical density values of RECK protein expression in early pregnancy group and term pregnancy group were 1.35±0.14 and 2.68±0.26, respectively, while MMP-2 activation ratio was contrary to RECK protein expression and decreased with the gestation time （P〈0.01）. The MMP-2 activation ratios of early pregnancy group and term pregnancy group were 0.46±0.05 and 0.10±0.02, respectively. The expression of the tumor inhibitory gene RECK was positively related with the invasion ability of trophoblasts, while the invasion gene MMP-2 was negatively related with the ability. The interaction between RECK and MMP-2 may play an important role in the regulation of the trophoblast invasion in early pregnancy.

关键词： RECK matrix metalloproteinase-2 placenta invasion

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Vascular Endothelial Growth Factorl65-regulated Nasopharyngeal Carcinoma Cell Lines Invasion and Migration Involve Expression and Activation of matrix metalloproteinase-2

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2006年第5期26卷 621-624页

作者：王彦君孔维佳乐建新孙大为李伟姚琪孙宇董继华 Department of OtorhinolaryngologyTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430022China Laboratory of Virology Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430022China

The effect of vascular endothelial growth factor （VEGF） overexpression on matrix metalloproteinase-2 （MMP-2） in nasopharyngeal carcinoma （NPC） cells in vitro and the possible mechanism involved were investigated, and the correlation between the expression of VEGF and MMP-2 in NPC evaluated. The NPC cells were transfected with PAd-trackVEGF165 plasmid. The expression levels of VEGF and MMP-2 mRNA and protein in NPC cells were detected by semi-quantitative RT-PCR and Western blot respectively. It was found that the expression of VEGF and MMP-2 mRNA and protein was significantly increased in NPC cells after transfection of VEGF 165. It was concluded that the expression of VEGF was correlated to the in vitro invasion of NPC cells, and the induction of MMP-2 by VEGF was a key process of NPC cell invasion.

关键词： nasopharyngeal carcinoma cells vascular endothelial growth factor matrix metalloproteinase-2 gene transfection

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Effects of valsartan on matrix metalloproteinase-2 and tissue inhibitor of matrix metalloproteinase-2 in atrial fibrillation patients

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South China Journal of Cardiology 2010年第1期11卷 15-19页

作者：裴晓阳潘莹颜雯胡雪松 Department of Cardiology the Fourth People's Hospital Shenzhen China Department of Cardiology Longgang District People's Hospital Shenzhen China

Background To observe the effects of valsartan on matrix metalloproteinase-2 （MMP-2） and tissue inhibitor of matrix metalloproteinase-2 （TIMP-2） in atrial fibrillation patients. Methods 30 patients with non-vavular atrial fibrillation（NVAF） as atrial fibrillation group （AF group） were randomly divided into two groups： 15 patients were in therapy group （valsartan 80 mg qd） and 15 patients were in control group. Plasma MMP-2 and TIMP-2 level between therapy and control group before and after treatment and 30 normal patients as normal group （SN group） were measured by ELISA. Results High levels of MMP-2 were observed in AF group comparing with normal group （P0.01）, and the level of TIMP-2 was significantly lower （P0.01）. There was no difference between therapy group and control group in MMP-2 and TIMP-2 before treatment. However,after three months treatment, MMP-2 in therapy group was significantly lower than control group（P0.001）. While in therapy group there was a significant difference before and after in MMP-2（P0.01） and TIMP-2 （P0.05）. Conclusions There are high level of MMP-2 and lower TIMP-2 in NVAF patients. Valsartan might inhibit the process of non-vavular atrial fibrillation by down regulating of MMP-2 and up regulating of TIMP-2.

关键词： non-vavular atrial fibrillation angiotensinⅡreceptor antagonist matrix metalloproteinase-2 matrix metalloproteinase-2 renin angiotensin system

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