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Parstatin (mouse)

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Parstatin, a 41-mer peptide which is cleaved upon activation of Proteinase-Activated Receptor 1, attenuates endothelial cell migration and proliferation (IC50 ~ 20 μM), and induces cell cycle arrest. It promotes activation of caspase-3 and exhibits pro-apoptotic activity in vitro.

Category

Functional Peptides

Catalog number

BAT-013364

CAS number

1065756-01-5

Molecular Formula

C189H326N58O57S3

Molecular Weight

4419.19

Specification
Reference Reading

IUPAC Name

(4S)-4-[[(2S)-1-[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-1-[2-[[(2R)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-1-[2-[[(2S)-2-amino-4-methylsulfanylbutanoyl]amino]acetyl]pyrrolidine-2-carbonyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-4-methylpentanoyl]amino]-4-methylpentanoyl]amino]-3-methylpentanoyl]amino]-3-methylbutanoyl]amino]propanoyl]amino]-4-methylpentanoyl]amino]acetyl]amino]-4-methylpentanoyl]amino]-3-hydroxypropanoyl]amino]-4-methylpentanoyl]amino]-3-sulfanylpropanoyl]amino]acetyl]pyrrolidine-2-carbonyl]amino]-4-methylpentanoyl]amino]-4-methylpentanoyl]amino]-3-hydroxypropanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-3-methylbutanoyl]pyrrolidine-2-carbonyl]amino]-4-methylsulfanylbutanoyl]amino]-3-hydroxypropanoyl]amino]-5-oxopentanoyl]pyrrolidine-2-carbonyl]amino]-5-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S,3R)-1-[[(2S)-1-[[(2S)-1-[[(2S,3R)-1-[[(2S)-1-[[(2S)-4-amino-1-[(2S)-2-[[(1S)-4-carbamimidamido-1-carboxybutyl]carbamoyl]pyrrolidin-1-yl]-1,4-dioxobutan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-1-oxopropan-2-yl]amino]-3-carboxy-1-oxopropan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-5-oxopentanoic acid

Synonyms

H-Met-Gly-Pro-Arg-Arg-Leu-Leu-Ile-Val-Ala-Leu-Gly-Leu-Ser-Leu-Cys-Gly-Pro-Leu-Leu-Ser-Ser-Arg-Val-Pro-Met-Ser-Gln-Pro-Glu-Ser-Glu-Arg-Thr-Asp-Ala-Thr-Val-Asn-Pro-Arg-OH; L-methionyl-glycyl-L-prolyl-L-arginyl-L-arginyl-L-leucyl-L-leucyl-L-isoleucyl-L-valyl-L-alanyl-L-leucyl-glycyl-L-leucyl-L-seryl-L-leucyl-L-cysteinyl-glycyl-L-prolyl-L-leucyl-L-leucyl-L-seryl-L-seryl-L-arginyl-L-valyl-L-prolyl-L-methionyl-L-seryl-L-glutaminyl-L-prolyl-L-alpha-glutamyl-L-seryl-L-alpha-glutamyl-L-arginyl-L-threonyl-L-alpha-aspartyl-L-alanyl-L-threonyl-L-valyl-L-asparagyl-L-prolyl-L-arginine

Related CAS

1065755-99-8 (human)

Appearance

White Lyophilized Solid

Purity

≥98%

Sequence

MGPRRLLIVALGLSLCGPLLSSRVPMSQPESERTDATVNPR

Storage

Store at -20°C

Solubility

Soluble in Water (1 mg/ml)

InChI

InChI=1S/C189H326N58O57S3/c1-29-98(22)144(240-165(284)119(76-94(14)15)226-161(280)115(72-90(6)7)224-153(272)104(40-30-58-203-185(193)194)214-152(271)105(41-31-59-204-186(195)196)218-171(290)128-45-35-63-243(128)136(258)80-209-149(268)103(190)56-68-306-27)178(297)237-141(95(16)17)176(295)212-99(23)147(266)223-113(70-88(2)3)150(269)208-79-135(257)213-114(71-89(4)5)160(279)233-125(85-251)169(288)227-117(74-92(10)11)164(283)236-127(87-305)151(270)210-81-137(259)244-64-36-46-129(244)172(291)228-118(75-93(12)13)162(281)225-116(73-91(8)9)163(282)234-126(86-252)170(289)235-123(83-249)166(285)216-106(42-32-60-205-187(197)198)157(276)239-143(97(20)21)183(302)247-67-39-49-132(247)174(293)220-110(57-69-307-28)156(275)232-124(84-250)168(287)221-111(50-53-133(191)255)181(300)245-65-37-47-130(245)173(292)219-109(52-55-139(262)263)155(274)231-122(82-248)167(286)217-108(51-54-138(260)261)154(273)215-107(43-33-61-206-188(199)200)158(277)242-145(101(25)253)179(298)229-120(78-140(264)265)159(278)211-100(24)148(267)241-146(102(26)254)180(299)238-142(96(18)19)177(296)230-121(77-134(192)256)182(301)246-66-38-48-131(246)175(294)222-112(184(303)304)44-34-62-207-189(201)202/h88-132,141-146,248-254,305H,29-87,190H2,1-28H3,(H2,191,255)(H2,192,256)(H,208,269)(H,209,268)(H,210,270)(H,211,278)(H,212,295)(H,213,257)(H,214,271)(H,215,273)(H,216,285)(H,217,286)(H,218,290)(H,219,292)(H,220,293)(H,221,287)(H,222,294)(H,223,266)(H,224,272)(H,225,281)(H,226,280)(H,227,288)(H,228,291)(H,229,298)(H,230,296)(H,231,274)(H,232,275)(H,233,279)(H,234,282)(H,235,289)(H,236,283)(H,237,297)(H,238,299)(H,239,276)(H,240,284)(H,241,267)(H,242,277)(H,260,261)(H,262,263)(H,264,265)(H,303,304)(H4,193,194,203)(H4,195,196,204)(H4,197,198,205)(H4,199,200,206)(H4,201,202,207)/t98-,99-,100-,101+,102+,103-,104-,105-,106-,107-,108-,109-,110-,111-,112-,113-,114-,115-,116-,117-,118-,119-,120-,121-,122-,123-,124-,125-,126-,127-,128-,129-,130-,131-,132-,141-,142-,143-,144-,145-,146-/m0/s1

InChI Key

SVAINNLHALEEHP-HQNSSEMESA-N

Canonical SMILES

CCC(C)C(C(=O)NC(C(C)C)C(=O)NC(C)C(=O)NC(CC(C)C)C(=O)NCC(=O)NC(CC(C)C)C(=O)NC(CO)C(=O)NC(CC(C)C)C(=O)NC(CS)C(=O)NCC(=O)N1CCCC1C(=O)NC(CC(C)C)C(=O)NC(CC(C)C)C(=O)NC(CO)C(=O)NC(CO)C(=O)NC(CCCNC(=N)N)C(=O)NC(C(C)C)C(=O)N2CCCC2C(=O)NC(CCSC)C(=O)NC(CO)C(=O)NC(CCC(=O)N)C(=O)N3CCCC3C(=O)NC(CCC(=O)O)C(=O)NC(CO)C(=O)NC(CCC(=O)O)C(=O)NC(CCCNC(=N)N)C(=O)NC(C(C)O)C(=O)NC(CC(=O)O)C(=O)NC(C)C(=O)NC(C(C)O)C(=O)NC(C(C)C)C(=O)NC(CC(=O)N)C(=O)N4CCCC4C(=O)NC(CCCNC(=N)N)C(=O)O)NC(=O)C(CC(C)C)NC(=O)C(CC(C)C)NC(=O)C(CCCNC(=N)N)NC(=O)C(CCCNC(=N)N)NC(=O)C5CCCN5C(=O)CNC(=O)C(CCSC)N

1. Parstatin suppresses ocular neovascularization and inflammation

Hu Huang, Panagiotis Vasilakis, Sotirios P Gartaganis, Stanley A Vinores, Katerina Geronatsiou, Ji-Kui Shen, Xiufeng Zhong, Helen Papadaki, Michael E Maragoudakis, Nikos E Tsopanoglou Invest Ophthalmol Vis Sci . 2010 Nov;51(11):5825-32. doi: 10.1167/iovs.10-5576.

Purpose:Parstatin is a 41-mer peptide formed by proteolytic cleavage on activation of the PAR1 receptor. The authors recently showed that parstatin is a potent inhibitor of angiogenesis. The purpose of the present study was to evaluate the therapeutic effect of parstatin on ocular neovascularization.Methods:Choroidal neovascularization was generated in mice using laser-induced rupture of Bruch's membrane and was assessed after 14 days after perfusion of FITC-dextran. Oxygen-induced retinal neovascularization was established in neonatal mice by exposing them to 75% O(2) at postnatal day (P)7 for 5 days and then placing them in room air for 5 days. Evaluation was performed on P17 after staining with anti-mouse PECAM-1. The effect of parstatin was tested after intravitreal administration. The effects of subconjunctival-injected parstatin on corneal neovascularization and inflammation in rats were assessed 7 days after chemical burn-induced corneal neovascularization. Retinal leukostasis in mice was assessed after perfusion with FITC-conjugated concanavalin A.Results:Parstatin potently inhibited choroidal neovascularization with an IC(50) of approximately 3 μg and a maximum inhibition of 59% at 10 μg. Parstatin suppressed retinal neovascularization with maximum inhibition of 60% at 3 μg. Ten-microgram and 30-μg doses appeared to be toxic to the neonatal retina. Subconjunctival parstatin inhibited corneal neovascularization, with 200 μg the most effective dose (59% inhibition). In addition, parstatin significantly inhibited corneal inflammation and VEGF-induced retinal leukostasis. In all models tested, scrambled parstatin was without any significant effect.Conclusions:Parstatin is a potent antiangiogenic agent of ocular neovascularization and may have clinical potential in the treatment of angiogenesis-related ocular disorders.

2. Anti-Parstatin Promotes Angiogenesis and Ameliorates Left Ventricular Dysfunction during Pressure Overload

Sathnur Basappa Pushpakumar, Nithya Narayanan, Srikanth Givvimani, Suresh C Tyagi Int J Biomed Sci . 2014 Mar;10(1):1-7.

Parstatin, a novel protease activated receptor-1 (PAR-1) derived peptide is a potent inhibitor of angiogenesis. We and others have reported that imbalance between angiogenic growth factors and anti-angiogenic factors results in transition from compensatory cardiac hypertrophy to heart failure in a pressure overload condition. Though cardio protective role of parstatin was shown previously in ischemic cardiac injury, its role in pressure overload cardiac injury is yet to unveil. We hypothesize that supplementing anti-parstatin antibody during pressure overload condition augments angiogenesis and ameliorate left ventricular dysfunction and heart failure. To verify this, we created ascending aortic banding in mice to mimic pressure overload condition and then treated mice with anti-parstatin antibody. Left ventricular function was assessed by echocardiography and pressure-volume loop study. Angiogenic growth factors and anti-angiogenic factors along with MMP-2,-9 were evaluated by western blot and immunohistochemistry.Results:our results showed an improved left ventricular function in anti-parstatin treated aortic banding hearts compared to their corresponding wild type controls. Expression of angiogenic growth factor, VEGF, MMP-2 and CD31 expression was increased in treated aortic banding hearts compared to their corresponding wild type controls. Our results suggest that treating pressure overload mice with anti-parstatin antibody augments angiogenesis and ameliorates left ventricular dysfunction.

3. Hydrogen sulfide mitigates cardiac remodeling during myocardial infarction via improvement of angiogenesis

Paras K Mishra, David Lominadze, Suresh C Tyagi, Natia Qipshidze, Naira Metreveli Int J Biol Sci . 2012;8(4):430-41. doi: 10.7150/ijbs.3632.

Exogenous hydrogen sulfide (H2S) leads to down-regulation of inflammatory responses and provides myocardial protection during acute ischemia/reperfusion injury; however its role during chronic heart failure (CHF) due to myocardial infarction (MI) is yet to be unveiled. We previously reported that H2S inhibits antiangiogenic factors such, as endostatin and angiostatin, but a little is known about its effect on parstatin (a fragment of proteinase-activated receptor-1, PAR-1). We hypothesize that H2S inhibits parstatin formation and promotes VEGF activation, thus promoting angiogenesis and significantly limiting the extent of MI injury. To verify this hypothesis MI was created in 12 week-old male mice by ligation of left anterior descending artery (LAD). Sham surgery was performed except LAD ligation. After the surgery mice were treated with sodium hydrogen sulfide (30 μmol/l NaHS, a donor for H2S, in drinking water) for 4 weeks. The LV tissue was analyzed for VEGF, flk-1 and flt-1, endostatin, angiostatin and parstatin. The expression of VEGF, flk-1 and flt-1 were significantly increased in treated mice while the level of endostatin, angiostatin and parstatin were decreased compared to in untreated mice. The echocardiography in mice treated with H2S showed the improvement of heart function compared to in untreated mice. The X-ray and Doppler blood flow measurements showed enhancement of cardiac-angiogenesis in mice treated with H2S. This observed cytoprotection was associated with an inhibition of anti-angiogenic proteins and stimulation of angiogenic factors. We established that administration of H2S at the time of MI ameliorated infarct size and preserved LV function during development of MI in mice. These results suggest that H2S is cytoprotective and angioprotective during evolution of MI.