Biomedical subjects

Hai-Yan Zhou

Publications and source records attributed to Hai-Yan Zhou.

8 recordsLinked to original sources

PubMed2006

Site-specific in vivo calcification and osteogenesis stimulated by bone sialoprotein.

Bone sialoprotein (BSP) is one of the major non-collagenous glycosylated phosphoproteins of the extracellular matrix in bone. In vitro studies suggest that BSP may play important roles in the initiation and/or growth of calcium-phosphate crystals. To investigate the potential role of BSP in more complex in vivo environments, we implanted purified bovine BSP with type-I collagen as a carrier into surgically created rat calvarial defects and thoracic subcutaneous pouches. The responses to the implants were assessed by histochemistry, immunohistochemistry, in situ hybridization, quantitative real-time PCR, and biochemical analyses. BSP-collagen, but not collagen alone, elicited mineral deposition in the matrix of proliferating cells near the dura at days 4-5 followed by osteoblast differentiation and synthesis of new bone in the mid-portion of the calvarial defects. In contrast, implantation of BSP-collagen into subcutaneous pouches did not induce calcification or osteogenesis over the same experimental period. We explored the underlying mechanisms for the site-specific responses to BSP-collagen implants and found that higher levels of calcium content and alkaline phosphatase activity at the cranial site at days 2-5 were associated with the BSP-mediated calcification. We also found that BSP stimulated osteoblast differentiation through up-regulation of cbfa1 and osterix, key transcription factors of osteoblast differentiation, which occurred in the calvarial defects but not in the subcutaneous tissue. These results demonstrate that BSP stimulates calcification and osteogenesis in a site-specific manner, and that local environment and the specificities of responding cells may play critical roles in the function of BSP in vivo.

Alkaline Phosphatase↗

PubMed2006

Heat shock proteins reduce alpha-synuclein aggregation induced by MPP+ in SK-N-SH cells.

Alpha-synuclein has been implicated in the pathogenesis of Parkinson's disease (PD). Heat shock proteins (HSPs) can reduce protein misfolding and accelerate the degradation of misfolded proteins. 1-methyl-4-phenylpyridinium ion (MPP+) is the compound responsible for the PD-like neurodegeneration caused by MPTP. In this study, we found that MPP+ could increase the expression of alpha-synuclein mRNA but could not elevate proteasome activity sufficiently, leading to alpha-synuclein protein accumulation followed by aggregation. Both HSPs and HDJ-1, a homologue of human Hsp40, can inhibit MPP+-induced alpha-synuclein mRNA expression, promote ubiquitination and elevate proteasome activity. These findings suggest that HSPs may inhibit the MPP+-induced alpha-synuclein expression, accelerate alpha-synuclein degradation, thereby reducing the amount of alpha-synuclein protein and accordingly preventing its aggregation.

1-Methyl-4-phenylpyridinium↗

PubMed2006

Overexpression of CaHSP26 in transgenic tobacco alleviates photoinhibition of PSII and PSI during chilling stress under low irradiance.

A sweet pepper cDNA clone, CaHSP26 encoding the chloroplast (CP)-localized small heat shock protein (sHSP), was isolated and characterized with regard to its sequence, response to various temperatures and function in transgenic tobacco plants. The deduced amino acid sequence contained three highly conserved regions, showing high identities with other plant sHSPs. Expression of the CaHSP26 gene showed that the mRNA accumulation of CaHSP26 was induced by heat stress. Higher transcript levels were observed when sweet pepper leaves were treated at 42 degrees C for 3h. However, the expression of the CaHSP26 gene was not induced by chilling stress (4 degrees C) in the absence of heat shock (HS). But the transcripts were still detected at 48h at 4 degrees C after HS while not at 25 degrees C. The photochemical efficiency of PSII (Fv/Fm) and the oxidizable P700 in transgenic tobacco overexpressing CaHSP26 were higher than that in wild type tobacco during chilling stress under low irradiance. These results suggest that CP sHSP protein plays an important role in protection of PSII and PSI during chilling stress under low irradiance.

Acclimatization↗

PubMed2006

Economic burden of Parkinson's disease in a developing country: a retrospective cost analysis in Shanghai, China.

We investigated economic costs from patients with Parkinson's disease (PD) in Shanghai, China, which could be used as a baseline for future evaluations. Data were collected from 190 patients by interview during 1-year period. Direct medical care costs averaged approximately Chinese yuan, renminbi (RMB) 4,305 (USD 519, or EUR 410) per year per patient, of which drugs (RMB 2,677) accounted for the major costly component. Nonmedical direct costs were much less than direct health care costs, averaging approximately RMB 3,301 (USD 398, or EUR 314). Costs due to loss of productivity averaged approximately RMB 73 (USD 8.8, or EUR 7.0) per patient per year. Taken together, the overall mean annual cost for PD in our series was approximately RMB 7,679 (USD 925, or EUR 731), and these costs accounted for around half of the mean annual income. Total cost was significantly associated with the disease severity and the frequency of outpatient visits. In addition, levodopa equivalent dose (LED) and the number of drugs being taken were also closely related with the drug cost. The results indicate that the economic burden of Chinese PD patients is heavy.

Adult↗

PubMed2006

[A model for trans-translation].

Trans-translation is a mechanism that fixes stalled translation course. tmRNA is the core of trans-translation and it has dual function as a tRNA and a mRNA. tmRNA recognizes the ribosome carrying truncated mRNA with specificity under the help SmpB protein. It can be directed to A site by ribosomal protein S1. At first tmRNA prolongs the genetic message on the stalled mRNA, then termination codon stops peptide synthesis to form a nascent chain with the tag sequence. Finally, tmRNA-SmpB system frees stalled ribosomes and directs degradation of the products of these frustrated protein synthesis reactions. This paper introduces the most recent studies on trans-translation.

Escherichia coli↗

PubMed2005

PACAP protects neuronal differentiated PC12 cells against the neurotoxicity induced by a mitochondrial complex I inhibitor, rotenone.

In vivo and in vitro studies have suggested a neuroprotective role for Pituitary adenylate cyclase activating polypeptide (PACAP) against neuronal insults. Here, we showed that PACAP27 protects against neurotoxicity induced by rotenone, a mitochondrial complex I inhibitor that has been implicated in the pathogenesis of Parkinson's disease (PD). The neuroprotective effect of PACAP27 was dose-dependent and blocked by its specific receptor antagonist, PACAP6-27. The effects of PACAP27 on rotenone-induced cell death were mimicked by dibutyryl-cAMP (db-cAMP), forskolin and prevented by the PKA inhibitor H89, the ERK inhibitor PD98059 and the p38 inhibitor SB203580. PACAP27 administration blocked rotenone-induced increases in the level of caspase-3-like activity, whereas could not restore mitochondrial activity damaged by rotenone. Thus, our results demonstrate that PACAP27 has a neuroprotective role against rotenone-induced neurotoxicity in neuronal differentiated PC12 cells and the neuroprotective effects of PACAP are associated with activation of MAP kinase pathways by PKA and with inhibition of caspase-3 activity; the signaling mechanism appears to be mediated through mitochondrial-independent pathways.

Animals↗

PubMed2005

Neuroprotection of Parkin against apoptosis is independent of inclusion body formation.

Loss-of-function mutations in the parkin gene are known to result in autosomal recessive juvenile parkinsonism, which causes selective degeneration of nigrostriatal dopaminergic neurons in the absence of Lewy bodies. Here, we show that overexpression of parkin protects PC12 cells from neurotoxin of the proteasome inhibitor lactacystin and increases the accumulation of ubiquitin-protein conjugates and the formation of ubiquitin-positive inclusions induced by lactacystin. However, the protective effect of parkin against lactacystin-induced apoptosis is not associated with its ability to promote the formation of ubiquitinated inclusions. It is likely that Lewy body formation may be only a compensatory mechanism of dopaminergic neurons attempting to counteract toxicity, and not the ultimate cause of neuronal death.

Animals↗

PubMed2003

High performance liquid chromatographic fingerprint evaluation of the quinolizidine alkaloids from commercial Radix Sophorae Flavescentis.

Fifteen commercial samples of Radix Sophorae Flavescentis were collected from different parts of China. HPLC analysis showed that the commercial samples all contained quinolizidine alkaloids and a total of nine chromatographic peaks were identified by referring to standard compounds, HPLC/MS analysis and comparison of the physicochemical data of the isolated peak with the literature. The contents of the major alkaloids were determined and the ratio of the major alkaloids contents was shown to be correlated with their source of origin. The commercial samples from China gave a distinct HPLC pattern showing the main alkaloids contents. The sample preparations were researched and the extraction conditions of the alkaloids were optimized. Reproducible HPLC fingerprints can be obtained for the quinolizidine alkaloids under the well-controlled extraction conditions. The HPLC fingerprint analysis method is suitable for the quality control of the Radix Sophorae Flavescentis and the standardization of phytomedicines.

Alkaloids↗