siRNA-mediated silencing of PAI-1 gene acts as a promoter over the recanalization of endothelial progenitor cells in rats with venous thrombosis.

With the changing lifestyle, venous thrombosis (VT) is becoming increasingly prevalent and poses a burden on the health economy. Endothelial progenitor cells (EPCs) are recruited into resolving VT. We aimed to investigate the effect of plasminogen activator inhibitor 1 (PAI-1) silencing on the recanalization of VT in rat EPCs. EPCs and VT rat models were cultured and treated with negative control-siRNA vector and PAI-1-siRNA vector, respectively. 4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, wound-healing test, and Matrigel-induced tubular experiment were performed to detect the ability of cell proliferation, migration, and EPCs lumen formation. Immunohistochemistry was used to observe the recanalization of thrombus. The messenger RNA (mRNA) and protein expression of PAI-1 and vascular endothelial growth factor (VEGF) were determined by reverse transcription quantitative polymerase chain reaction and Western blot analysis. PAI-1-siRNA enhances the luminal formation ability of EPCs and significantly promotes EPCs homing. In response to PAI-1 gene silencing, tissues from inferior vena cava displayed reduced mRNA and protein expression of PAI-1, increased VEGF expression as well as promoted lumen-like structures. PAI-1 gene silencing can promote the recanalization of VT by enhancement of the luminal formation ability of rats' EPCs.

Identification of candidate target genes for human peripheral arterial disease using weighted gene co­expression network analysis.

The aim of the present study was to identify the potential treatment targets of peripheral arterial disease (PAD) and provide further insights into the underlying mechanism of PAD, based on a weighted gene co­expression network analysis (WGCNA) method. The mRNA expression profiles (accession. no. GSE27034), which included 19 samples from patients with PAD and 18 samples from normal control individuals were extracted from the Gene Expression Omnibus database. Subsequently, the differentially expressed genes (DEGs) were obtained using the Limma package and the co­expression network modules were screened using the WGCNA approach. In addition, the protein­protein interaction network for the DEGs in the most significant module was constructed using Cytoscape software. Functional enrichment analyses of the DEGs in the most significant module were also performed using the Database for Annotation, Visualization and Integrated Discovery and Kyoto Encyclopedia of Genes and Genomes (KEGG) Orthology­Based Annotation System, respectively. A total of 148 DEGs were identified in PAD, which were used to construct the WGCN, in which two modules (gray module and turquoise module) were identified, with the gray module exhibiting a higher gene significance (GS) value than the turquoise module. In addition, a co­expression network was constructed for 60 DEGs in the gray module. The functional enrichment results showed that the DEGs in the gray module were enriched in five Gene Ontology terms and four KEGG pathways. For example, cyclin­dependent kinase inhibitor 1A (CDKN1A), FBJ murine osteosarcoma viral oncogene homolog (FOS) and prostaglandin­endoperoxide synthase 2 (PTGS2) were enriched in response to glucocorticoid stimulus. The results of the present study suggested that DEGs in the gray module, including CDKN1A, FOS and PTGS2, may be associated with the pathogenesis of PAD, by modulating the cell cycle, and may offer potential for use as candidate treatment targets for PAD.

catena-Poly[[zinc-bis-(µ-2-sulfido-1H-benzimidazol-3-ium-5-carboxyl-ato)-κO:S;κS:O] trihydrate].

In the title compound, {[Zn(C(8)H(5)N(2)O(2)S)(2)]·3H(2)O}(n), the Zn(II) atom, lying on a twofold rotation axis, is four-coordinated by two S atoms and two O atoms from four 2-sulfido-1H-benzimidazol-3-ium-5-carboxyl-ate (H(2)mbidc) ligands in a distorted tetra-hedral geometry. Two H(2)mbidc ligands bridge two Zn(II) atoms, generating a double-chain along [[Formula: see text]01]. Adjacent chains are linked by N-H⋯O and O-H⋯O hydrogen bonds, forming a three-dimensional supra-molecular network. One of the two water molecules also lies on a twofold rotation axis.

A novel parallel interpenetrating two-dimensional (4,4) network: poly[[mu2-1,4-bis(imidazol-1-ylmethyl)benzene](mu2-naphthalene-1,4-dicarboxylato)zinc(II)].

In the title coordination compound, [Zn(C(12)H(6)O(4))(C(14)H(14)N(4))](n), the two Zn(II) centers exhibit different coordination environments. One Zn(II) center is four-coordinated in a distorted tetrahedral environment surrounded by two carboxylate O atoms from two different naphthalene-1,4-dicarboxylate (1,4-ndc) anions and two N atoms from two distinct 1,4-bis(imidazol-1-ylmethyl)benzene (1,4-bix) ligands. The coordination of the second Zn(II) center comprises two N atoms from two different 1,4-bix ligands and three carboxylate O atoms from two different 1,4-ndc ligands in a highly distorted square-pyramidal environment. The 1,4-bix ligand and the 1,4-ndc anion link adjacent Zn(II) centers into a two-dimensional four-connected (4,4) network. The two (4,4) networks are interpenetrated in a parallel mode.

Poly[[µ(2)-1,4-bis-(imidazol-1-ylmeth-yl)benzene]bis-(µ(4)-cyclo-hexane-1,4-dicarboxyl-ato)dicobalt(II)].

In the title compound, [Co(2)(C(8)H(10)O(4))(2)(C(14)H(14)N(4))](n), the two Co(II) atoms are both five-coordinated by four carboxyl-ate O atoms, derived from two different cyclo-hexane-1,4-dicarboxyl-ate (chdc) ligands, and an N atom, derived from one end of a 1,4-bis-(imidazol-1-ylmeth-yl)benzene mol-ecule (1,4-bix), in a distorted square-pyramidal environment. Each end of the chdc ligand links pairs of Co(II) atoms into a paddle-wheel assembly, i.e. Co(2)(O(2)CR')(4); these are connected into rows because of the bridging nature of the chdc ligands, and the rows are further connected into a two-dimensional layer through the 1,4-bix ligands. The 1,4-bix ligand, which is disposed about a centre of inversion, is disorderd. Two positions were discerned for the -CH(2)(C(6)H(4))CH(2)- residue, with the major component having a site-occupancy factor of 0.512 (9).

catena-Poly[[[aqua-(pyrazino[2,3-f][1,10]phenanthroline)cadium(II)]-µ-4,4'-ethyl-enedibenzoato] N,N-dimethyl-formamide hemisolvate].

In the title compound, [Cd(C(16)H(10)O(4))(C(14)H(8)N(4))(H(2)O)]·0.5C(3)H(7)NO, the Cd(II) atom is six-coordinated by two N atoms from one pyrazino[2,3-f][1,10]phenanthroline ligand, three carboxyl-ate O atoms from two different 4,4'-ethyl-enedibenzoate ligands, and one water mol-ecule in a distorted octa-hedral environment. The two 4,4'-ethyl-enedibenzoate dianions are located on inversion centres bridging two neighboring Cd(II) centres. O-H⋯O hydrogen-bonding inter-actions further stabilize the crystal structure. The DMF molecule is equally disordered about a center of inversion.

catena-Poly[[[aqua-(1,10-phenanthro-line)zinc(II)]-µ-3,3'-(p-phenyl-ene)di-acrylato] hemihydrate].

In the title compound, {[Zn(C(12)H(8)O(4))(C(12)H(8)N(2))(H(2)O)]·0.5H(2)O}(n), each Zn(II) atom is six-coordinated by two N atoms from one 1,10-phenanthroline (phen), three carboxyl-ate O atoms from two different L ligands [H(2)L = 3,3'-(p-phenyl-ene)diacrylic acid] and one water mol-ecule in a distorted octa-hedral environment. The two L dianions are situated across inversion centres and bridge neighbouring Zn(II) centres, yielding a chain propagating parallel to [100]. O-H⋯O hydrogen bonds between the coordinated water molecule, the solvent water molecule (half-occupied) and the carboxylate O atoms further stabilize the structure.