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Li Cao

Publications and source records attributed to Li Cao.

59 records · Page 4Linked to original sources

Cationic liposome-mediated GDNF gene transfer after spinal cord injury.

Glial cell line-derived neurotrophic factor (GDNF) has been shown to protect cranial and spinal motoneurons, which suggests potential uses of GDNF in the treatment of spinal cord injury (SCI) and motor neuron disease. We examined neuroprotective effect of cationic liposome-mediated GDNF gene transfer in vivo on axonal regeneration and locomotor function recovery after SCI in adult rats. The mixture of DC-Chol liposomes and recombinant plasmid pEGFP-GDNF cDNA was injected after SCI. RT-PCR confirmed the increased expression of GDNF mRNA in the injected areas at 7 days after injection. The expression of EGFP-GDNF was observed in the cells around the injection locus by fluorescence microscope at least 4 weeks after injection. Four weeks after GDNF gene transfer, regeneration of the corticospinal tracts was assessed using anterograde tract tracing. There are more HRP labeling of corticospinal tract axons across the lesion in GDNF group compared with control group. In GDNF group, the maximum distance these labeled axons extended varied in different animals and ranged from 5 mm to approximately 9 mm from the lesion. In control group, no HRP labeled axons extended caudal to the lesion. The locomotion function of hindlimbs of rats was evaluated using inclined plane test and BBB locomotor scores. The locomotion functional scores in GDNF group were higher than that in control group within 1-4 weeks after SCI (p < 0.05). These data demonstrate that in vivo transfer of GDNF cDNA can promote axonal regeneration and enhance locomotion functional recovery, suggesting that cationic liposome-mediated delivery of GDNF cDNA may be a practical gene transfer method for traumatic SCI treatment.

Animals↗

Phosphoinositide-specific inositol polyphosphate 5-phosphatase IV inhibits Akt/protein kinase B phosphorylation and leads to apoptotic cell death.

Phosphoinositide-specific inositol polyphosphate 5- phosphatase IV has the affinity for PI(3,4,5)P(3) (K(m) = 0.65 microM) that is approximately 10-fold greater than the other inositol polyphosphate 5-phosphatases, which use this substrate including SHIP, OCRL, and 5ptase II, suggesting that it may be important in controlling intracellular levels of this metabolite. We created cell lines stably expressing the enzyme to study its effect on cell function. We found that overexpression of 5ptase IV in 293 cells caused the rapid depletion of both PI(4,5)P(2) and PI(3,4,5)P(3) in cells with corresponding increases in the products, PI(4)P and PI(3,4)P(2), changing the balance of two phosphoinositol products of phosphoinositide 3-kinase, PI(3,4)P(2) and PI(3,4,5)P(3), in the cell. One of the targets of these phosphoinositides is the serine/threonine kinase Akt, which plays an important role in the control of apoptosis. We were able to address the relative roles of PI(3,4)P(2) and PI(3,4,5)P(3) in the activation of Akt by selective depletion of these phosphoinositides in cells stably transfected with 5ptase IV and inositol polyphosphate 4-phosphatase (4ptase I). In cells transfected with 4ptase I, the level of PI(3,4)P(2) was reduced, and PI(3,4,5)P(3) was increased. Expression of the two enzymes had the opposite effect on the phosphorylation of Akt in response to stimulation with growth factors or heat shock. Akt phosphorylation was inhibited in cells expressing 5ptase IV but increased in 4ptase I cells and correlated with the intracellular level of PI(3,4,5)P(3) and not that of PI(3,4)P(2). The inhibition of Akt phosphorylation in cells expressing 5ptase IV makes them highly susceptible to FAS-induced apoptosis, whereas overexpressing of the 4ptase I protects cells from apoptosis. Our results place 5ptase IV as a relevant biological regulator of PI3K/Akt pathway in cells.

Apoptosis↗

Analysis and Molecular Cloning of Differentially Expressing Genes in Nasopharyngeal Carcinoma.

In order to further examine expression of cDNA fragments isolated by cDNA representational difference analysis(cDNA RDA) in nasopharyngeal carcinoma(NPC) biopsies and to clone those deregulated genes associated with NPC, RT-PCR and Northern blot were used to identify the differentially expressed cDNA fragments in NPC biopsies and confirm the transcript length of those genes, then a full-length cDNA sequences was cloned and its product was analyzed by bioinformatics. The results showed that AF091521, AF091520, AF152605 and AF091517 cDNA sequences had distinct expression difference between primary cultural normal nasopharyngeal epithelial cell and NPC biopsies, and AF091521, AF091517 genes all had two transcripts whose sizes were 1.5, 2.3 and 1.1, 1.4 kb respectively, while AF091520 and AF152605 gene expressed one transcript only, respectively, whose sizes were 1.6 and 2.2 kb. An AF091517 EST gene, named as NAG11, (GenBank accession number AF170307) was isolated by sequencing one EST clone, which encoded a transmembrane protein of 88 amino acid including three protein ATP-binding regions, two protein kinase C phosphorylation sites and two N-myristoylation sites. So it is further demonstrated that NPC is a disease with multiple gene alterations NAG11 gene is a candidate of putative tumor suppressor genes associated with NPC, whose down-expression may be involved in the development of NPC and NAG11 gene product may play a role in the transmembrane transport of ATP.

Journal Article↗

Giant cell arteritis in China: a prospective investigation.

The objective of this prospective study was to investigate further the clinical features of patients with giant cell (temporal) arteritis (GCA). All patients diagnosed from July 1999 to March 2001 at the Department of Neurology of the Second Xiangya Hospital in China were included. The final diagnosis was based on clinical manifestations, a temporal artery biopsy, response to steroid, and follow-up. The American College of Rheumatology (ACR) criteria for the classification of GCA were tested in the patients identified. Sixteen patients with GCA were identified; 13 (81.25%) patients fulfilled the 1990 ACR criteria for the classification of GCA. Clinical findings included the following: mean age at disease onset 43.13 years (range 28-60) and 81.25% of the patients under the age of 50 when the disease began; men 93.75%; the common initial symptoms including new headache 62.50% and.visual symptoms 18.75%; the common clinical findings at presentation including new headache 93.75%, temporal artery abnormality 81.25%, visual abnormality 56.25%, and fever 25.00%; raised erythrocyte sedimentation rate (ESR) 68.75%; and uncommon findings including jaw claudication, ptosis, fatigue, syncope, hemiparesis; all 16 patients underwent a temporal artery biopsy; inflammatory cell infiltration 68.75% in arterial wall, fragmented internal elastica 100.00%, fibrinoid necrosis 18.75%, smooth muscle cell changes 62.50%, and thrombosis in the lumen 31.25%. The mean time from symptom onset to suspicion of GCA or biopsy was 5.52 months (range 0.25-24.33); the initial diagnosis was wrong in 87.50% of patients. These examples are too small a number to permit definite conclusion. But the results suggest that GCA may not be a rare disorder in China, mean age at disease onset was relatively young, males may be more susceptible, the clinical features of GCA have not been widely appreciated yet, there was a delay between diagnosis and treatment, and initial diagnosis was wrong in many patients.

Adult↗