Altitude ; Animals ; CA1 Region, Hippocampal ; metabolism ; physiology ; Male ; Neural Cell Adhesion Molecules ; metabolism ; Rats ; Rats, Sprague-Dawley ; Time Factors

OBJECTIVETo explore the influences of the restoration of neural adhesion molecule NECL1 on the morphology, migration, and invasion of NECL1-deficient glioma cell lines.

METHODSScratch and Transwell assays were used to observe the cell migration and invasion, the activities of extracellular metalloproteinases were measured, and the cell morphology was observed. Astrocytes marker glial fibrillary acidic protein was detected by Western blot after the restoration of NECL1 in glioma U251 cell line.

RESULTSIn NECL1-deficient U251 glioma cell lines, migration and invasion were inhibited. The U251 cells was differentiated potentially to astrocytes, and glial fibrillary acidic protein was up-regulated after the restoration of the NECL1 expression.

CONCLUSIONAs a potential tumor repressor, the neural adhesion molecule NECL1 can inhibit the migration and invasion of glioma cell and induces its differentiation.

Brain Neoplasms ; metabolism ; pathology ; Cell Differentiation ; Cell Line, Tumor ; Cell Movement ; Glioma ; metabolism ; pathology ; Humans ; Neoplasm Invasiveness ; Neural Cell Adhesion Molecules ; metabolism

OBJECTIVETo observe the effects of flutamide (Flu) on the development of testicular germocytes in SD rats, and to establish a rat model for further researches on the maldevelopment of cryptorchidism gonocytes (Go).

METHODSPregnant SD rats were subcutaneously injected with Flu from gestational day (GD) 12 to 21 to establish a model of cryptorchidism. The testes of the newborns were harvested on postnatal day (PD) 1, 10, 20 and 80 for observation of their morphological and histological changes by HE staining and detection of the expression of neural cell adhesion molecules (NCAM) by immunohistochemistry and RT-PCR.

RESULTSFlu induced 43.9% (29/66) of cryptorchidism in the exposed rats. Significant differences were found in the testicular weight and organ coefficient between the Flu and the control groups on PD 20 and 80. Gos remained in the center of seminiferous tubules of the Flu-induced testis on PD 10, and in the center of seminiferous tubules in the cryptorchids' testicular tissues on PD 20 and 80. Immunohistochemistry showed the expression of NCAM on the membrane of the remaining Gos, and RT-PCR revealed significantly up-regulated expression of NCAM mRNA in the Flu-induced testes on PD 10 and 20 as compared with the controls (P < 0.05).

CONCLUSIONA rat model of Flu-induced cryptorchidism with remaining Gos was successfully established, which could be used to study the mechanism and management of the maldevelopment of cryptorchidism gonocytes.

Animals ; Cryptorchidism ; chemically induced ; pathology ; Female ; Flutamide ; adverse effects ; Male ; Neural Cell Adhesion Molecules ; metabolism ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Testis ; drug effects ; metabolism ; pathology

OBJECTIVETo investigate the role of cell adhesion molecule in the development and extramedullary infiltration (EI) of acute leukemia.

METHODSThe expressions of neural cell adhesion molecule (NCAM) gene, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule (VCAM-1) genes in 25 acute leukemia patients bone marrow cells were detected by microarray and reverse transcriptase-polymerase chain reaction (RT-PCR).

RESULTSThe expressions of NCAM, ICAM-1 and VCAM-1 gene were significantly higher in acute leukemia cells and leukemia cells with EI than in normal tissues and leukemia cells without EI, respectively, both by cDNA microarray and by RT-PCR.

CONCLUSIONThe cDNA microarray is a powerful technique in analysis of acute leukemia cells associated genes. High expressions of cell adhesion molecule genes might be correlated with leukemia pathogenesis and infiltration of acute leukemia cell.

Acute Disease ; Adolescent ; Adult ; Aged ; Bone Marrow Cells ; metabolism ; pathology ; Cell Adhesion Molecules ; genetics ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Intercellular Adhesion Molecule-1 ; genetics ; Leukemia, Myeloid ; genetics ; pathology ; Male ; Middle Aged ; Neural Cell Adhesion Molecules ; genetics ; Oligonucleotide Array Sequence Analysis ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; genetics ; pathology ; RNA, Messenger ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Vascular Cell Adhesion Molecule-1 ; genetics

It has been demonstrated that neural cell adhesion molecule (NCAM) is critical for the induction and maintenance of long term potentiation (LTP) in the CA1 region of rat hippocampus. In the present study, we investigated the changes in NCAM mRNA expression and NCAM protein level after the induction of LTP in vitro using the techniques of in situ hybridization and Western blot. The results showed that the number of NCAM mRNA positive labelled neurons significantly increased (76.6+/-11.5 neurons) 10 min after tetanus when the slope of fEPSP markedly increased. The level of NCAM protein also increased significantly (7.190+/-0.64 arbitrary unit/50 microg protein) 10 min after tetanus. The number of NCAM mRNA positive labelled neurons no longer changed (73.3+/-14.0) 1 h after tetanus, however, the NCAM protein level (9.031+/-0.71) at 1 h after tetanus was higher than that at 10 min after tetanus. Moreover, the NMDA receptor inhibitor AP-5, which blocked LTP, prevented the increase in NCAM mRNA expression and NCAM protein level. The results demonstrate that NCAM mRNA expression maintains a high level, whereas NCAM protein changes from a low level to a high level during induction and maintenance of LTP.
Animals ; Hippocampus ; metabolism ; physiology ; Long-Term Potentiation ; physiology ; Male ; Neural Cell Adhesion Molecules ; biosynthesis ; genetics ; RNA, Messenger ; biosynthesis ; genetics ; Rats ; Rats, Wistar

Combined hepatocellular carcinoma and cholangiocarcinoma (combined HCC-CC) is a rare subtype of primary liver cancer. We investigated the histopathologic features of transitional or intermediate areas in 21 combined HCC-CCs and immunophenotypes using different hepatic progenitor cell markers (CK7, CK19, c-kit, NCAM, and EpCAM). Major histologic findings of transitional or intermediate areas of 21 combined HCC-CCs included strands/trabeculae of small, uniform, oval-shaped cells with scant cytoplasm and hyperchromatic nuclei embedded within an abundant stroma, small cells with an antler-like anastomosing pattern, and solid nests of intermediate hepatocyte-like cells surrounded by small cells in periphery, in order of frequency. The intermediate area of one tumor was composed predominantly of spindle cells arranged in short fascicles. Immunophenotype of tumor cells with intermediate morphology suggested a progenitor cell origin for this tumor. Clinical findings of combined HCC-CC showed a closer resemblance with those of HCC than those of CC. In univariate analysis, tumor size, TNM stage, and serum alpha-fetoprotein levels showed a significant association with poor patient survival. Serum alpha-fetoprotein level was an independent prognostic indicator in multivariate analysis. In conclusion, an awareness of the clinicopathologic features, specifically the various morphologic features of intermediate areas in this tumor, is essential for prevention of potential misdiagnosis as another tumor.
Adult ; Aged ; Antigens, Neoplasm/metabolism ; Carcinoma, Hepatocellular/*pathology ; Cell Adhesion Molecules/metabolism ; Cholangiocarcinoma/*pathology ; Female ; Humans ; Immunophenotyping ; Keratin-19/metabolism ; Keratin-7/metabolism ; Liver Neoplasms/*pathology ; Male ; Middle Aged ; Neural Cell Adhesion Molecules/metabolism ; Prognosis ; Proto-Oncogene Proteins c-kit/metabolism ; alpha-Fetoproteins/analysis

OBJECTIVETo study the impact of low-level lead exposure on neural cell adhesion molecule (NCAM) expression of primarily cultured hippocampal neurons.

METHODSWistar rats gestated at 18th day were anaesthetized and paunched to get the pups, the hippocampi of the pups were separated and the hippocampal neurons were primarily cultured. After co-cultivated with different dosage of PbCl(2), the NCAM expression of the neurons were tested with Western blotting at different culture time.

RESULTSNormally, the expression of NCAM at the 1st culture day was very low and its integral obsorbency density was 14; the climax expression time of NCAM of the cultured hippocampal neurons was 3rd to 5th cultured day, and their integral obsorbency density were 2 542 to 2 580; henceforth, the NCAM expression declined. NCAM expression was inhibited significantly by lead during the 2nd to 4th cultured day, and dose-response relationship was observed. The inhibition of lead weakened along with the cultured time prolonged, at 5th cultured day, it disappeared, and the NCAM expression of 10(-2), 10(-3) and 10(-4) mmol/L groups even exceeded the control groups. After that, the expression of NCAM in all groups began to decline, and the dose-response relationship of lead to the NCAM expression was observed again.

CONCLUSIONLow-level lead might significantly inhibit the NCAM expression of the primarily cultured Wistar rats' hippocampal neurons, and might delay the climax NCAM expression time.

Animals ; Animals, Newborn ; Cell Separation ; Cells, Cultured ; Dose-Response Relationship, Drug ; Female ; Hippocampus ; cytology ; drug effects ; metabolism ; Lead ; toxicity ; Neural Cell Adhesion Molecules ; biosynthesis ; genetics ; Neurons ; cytology ; Pregnancy ; Rats ; Rats, Wistar

OBJECTIVETo study the effects of astragalan (AG) on the expression of the neural cell adhesion molecule(NCAM) and c-fos of hippocampus CA1 region after the ischemic brain injury in rats.

METHODSOne hundred male Wistar rats (180-220 g) were divided into ten groups randomly, they were sham operated group (SOG, n = 10), three model group(MG-ld, 3d, 7d, n = 10), as well as three low and high dose astragalan treatment groups (L/H-AGTG-1d, 3d, 7d, n = 10), respectively. And then, middle cerebral artery of MG and AGTG were intercepted by operation inducing brain injured. Their cerebral blood vessel were reperfused on 1, 2, 3 d, respectively, after the L/H-AGTG were treated with the AG (5 mg/kg and 15 mg/kg, ip). After neurologic impairment(NIP) was scored, animals were decapitated to take out hippocampus for counting apoptosis , determining the expression of the NCAM and c-fos by immunohistochemistry method and RT-PCR semiquantitative analysis, respectively.

RESULTSThe NIP scores and apoptotic cell of the L-AGTG and H-AGTG were significantly lower than MG (P < 0.05 or P < 0.01). The expression of NCAM and c-fos were significantly higher than the MG (P < 0.05 or P < 0.01).

CONCLUSIONAstragalan could improve significantly neural function of ischemia brain injury in rats,the mechanism concerned probably with blocking or reversing apoptosis of hippocampus by promoting the expression of the NCAM and c-fos of hippocampus CA1 region.

Animals ; Apoptosis ; drug effects ; Astragalus membranaceus ; chemistry ; Brain Ischemia ; metabolism ; pathology ; CA1 Region, Hippocampal ; cytology ; Kaempferols ; pharmacology ; Male ; Neural Cell Adhesion Molecules ; metabolism ; Neurons ; drug effects ; Neuroprotective Agents ; pharmacology ; Polysaccharides ; pharmacology ; Rats ; Rats, Wistar

OBJECTIVEThis study explored the effects of levetiracetam (LEV) on the expression of nerve cell adhesion molecule (NCAM) and growth-associated protein 43 (GAP-43) mRNA in the hippocampus of rats with epilepsy induced by lithium-pilocarpine (Li-PILO) in order to provide a basis for investigating the antiepileptic mechanism of LEV and its doseresponse.

METHODSForty-eight Wistar rats were randomly divided into a normal control, a Li-PILO model and two LEV treatment groups (LEV: 150 and 300 mg/kg) (n=12 each). The LEV treatment groups received LEV by intragastric administration 6 hrs after status epilepticus (once daily for 2 two weeks). The expressions of NCAM and GAP-43 mRNA in the hippocampus was determined by real-time PCR.

RESULTSThe expression of NCAM and GAP-43 mRNA in the Li-PILO model group was significantly higher than in the normal control group (P<0.05). LEV treatment of 150 and 300 mg/kg significantly decreased the expression of NCAM and GAP-43 mRNA compared with the Li-PILO model group (P<0.05). The LEV treatment group at the dose of 300 mg/kg showed significantly lower expression of NCAM and GAP-43 mRNA than the 150 mg/kg LEV treatment group (P<0.05).

CONCLUSIONSLi-PILO can up-regulate the expressions of NCAM and GAP-43 mRNA in the hippocampus of rats with epilepsy. LEV can inhibit the expression of NCAM and GAP-43 mRNA and the effect is associated with the dose of LEV.

Animals ; Anticonvulsants ; therapeutic use ; Epilepsy ; drug therapy ; metabolism ; GAP-43 Protein ; genetics ; Hippocampus ; metabolism ; Male ; Neural Cell Adhesion Molecules ; genetics ; Piracetam ; analogs & derivatives ; pharmacology ; therapeutic use ; RNA, Messenger ; analysis ; Rats ; Rats, Wistar

Rat hippocampal precursor cells isolated from hippocampi of embryonic day 16.5 (E16.5) rat embryos were found to proliferate in the presence of basic fibroblast growth factor. Addition of soluble neural cell adhesion molecule (NCAM) to these precursor cells reduced cell proliferation in a dose dependent manner and enhanced the induction of precursor cells' differentiation to the neuronal lineage. Given these findings that NCAM induces the differentiation of hippocampal precursor cells, we investigated possible effects of NCAM on the expression of basic helix-loop-helix (bHLH) transcription factors during the differentiation. Soluble NCAM upregulated the transcription of bHLH transcription factors, neurogenin1 and NeuroD, but decreased HES5. Western blot analysis showed that NCAM increased the expression levels of CaMKII, p-MAPK, GluR1 and NR1 but decreased p-STAT3. These results support a role for NCAM in the inhibition of proliferation and the induction of neural differentiation of hippocampal neural precursor cells, and act as developmental regulators of the bHLH families, ultimately leading to the generation of glutamatergic neural cell types in the differentiation of hippocampal precursor cells.
Animals ; Apoptosis/drug effects ; Cell Differentiation/*drug effects ; Cell Division/drug effects ; Cell Lineage/drug effects ; Cells, Cultured ; Helix-Loop-Helix Motifs ; Hippocampus/*cytology/*drug effects ; Neural Cell Adhesion Molecules/*pharmacology ; Neurons/cytology/*drug effects/metabolism ; RNA, Messenger/genetics/metabolism ; Rats ; Receptors, Glutamate/*metabolism ; Signal Transduction ; Stem Cells/cytology/*drug effects ; Transcription Factors/genetics/metabolism