[Advances of Researchs on Molecular Mechanisms of Mesenchymal Stem Cells and Their Exosomes in Angiogenesis--Review].

Mesenchymal stem cells (MSC) have the potential of multi-directional differentiation, and can recruit endothelial cells, promote their proliferation, migration and angiogenesis, improve blood perfusion and oxygen suppliment, and repair damaged tissue. Exosome secreted by MSC contain mother cell-specific proteins, lipids and nucleic acids, and acts as signaling molecule, playing an important role in cell communication, thereby altering target cell function. In this review, the biological characteristics of MSC and its exosome, the mechanism of promoting vascular regeneration in patients with ischemic diseases, and the mechanism of hypoxia-inducible factor-1α（HIF-1α） in the vascular ischemia of ischemic diseases are all summarized briefly.

Correlation of CDC42 Activity with Cell Proliferation and Palmitate-Mediated Cell Death in Human Umbilical Cord Wharton's Jelly Derived Mesenchymal Stromal Cells.

RHO GTPases regulate cell migration, cell-cycle progression, and cell survival in response to extracellular stimuli. However, the regulatory effects of RHO GTPases in mesenchymal stromal cells (MSCs) are unclear. Herein, we show that CDC42 acts as an essential factor in regulating cell proliferation and also takes part in lipotoxic effects of palmitate in human umbilical cord Wharton's jelly derived MSCs (hWJ-MSCs).

[Palmitate induces apoptosis and endoplasmic reticulum stress in human umbilical cord-derived mesenchymal stem cells].

The saturated free fatty acid (FFA), palmitate, could induce apoptosis in various cell types, but little is known about its effects on human umbilical cord-derived mesenchymal stem cells (hUC-MSCs). Here, we investigated whether palmitate induced apoptosis and endoplasmic reticulum (ER) stress in hUC-MSCs. hUC-MSCs were stained by labeled antibodies and identified by flow cytometry.

BMSCs reduce rat granulosa cell apoptosis induced by cisplatin and perimenopause.

Background: The objective of this study was to evaluate the effect of bone marrow mesenchymal stem cells (BMSCs) on the apoptosis of granulosa cells (GCs) in rats.

Results: Cisplatin increased GC apoptosis from 0.59% to 13.

[A novel missense mutation resulting in X-linked adrenoleukodystrophy in female heterozygotes of a Chinese family].

Objective: To identify ABCD1 gene mutation in a Chinese family with three heterozygous female patients.

Methods: Four fragments covering the entire coding sequence of the ABCD1 gene from one of the female patients were amplified by reverse transcription-PCR. The PCR products were directly sequenced.

Microarray analysis of gene-expression profile in hepatocellular carcinoma cell, BEL-7402, with stable suppression of hLRH-1 via a DNA vector-based RNA interference.

To establish a cell line with a permanent suppression of hLRH-1 in this study, a stable RNAi vector (pSineohLRH-1) targeting hLRH-1 was constructed and introduced into hepatocellular carcinoma cell, BEL-7402. By semiquantitative RT-PCR analysis, the expression of hLRH-1 in BEL-7402 cells carrying pSineohLRH-1 was shown to be significantly suppressed by up to approximately 60%. In addition, microarray analysis was carried out to assess the extent of altered gene expression in BEL-7402 cells with stable knockdown of hLRH-1.

[Avoiding the interference of ABCD1 pseudogenes in the molecular diagnosis of X-linked adrenoleukodystrophy by double amplification refractory mutation system].

Objective: To avoid the interference of ABCD1 pseudogenes, the amplification refractory mutation system (ARMS) was used to analyze the mutation of ABCD1 gene in the molecular diagnosis of X-linked adrenoleukodystrophy (ALD).

Methods: The upstream primers (wild primer and mutation primer) were designed according to the principle of primer-design in ARMS. In addition, a common downstream primer was designed in the same way to discriminate ABCD1 gene from its prologous pseudogenes.

Prenatal molecular diagnosis of adrenoleukodystrophy.

Objective: To carry out prenatal diagnosis on two fetuses of different pedigrees with X-linked adrenoleukodystrophy (ALD).

Methods: The amniotic fluid was obtained with the help of a clinical doctor and the genomic DNA was isolated from it. Maternal DNA contamination was excluded by fluorescent STR profiling, The R617G mutation found in the first pedigree was searched in genomic DNA of amniotic fluid cells (AFC) from fetus 1 by amplification refractory mutation system (ARMS) and dot DNA hybridization while the P534R mutation found in pedigree 2 was analyzed in the AFC genomic DNA of fetus 2 by restrictive digestion with Hae II and DNA direct sequencing.

[Mutational analysis of three Chinese pedigrees with adrenoleukodystrophy].

Objective: To identify the mutational genotype of three Chinese families with X-linked adrenoleukodystrophy (X-ALD: MIM#300100).

Methods: Total RNA was extracted from the peripheral blood leukocytes of patients 1, 2 and the mother of patient 3, using RNA blood Mini kit (QIAGEN). After reverse transcription, cDNA was amplified in four overlapping segments.