[Show abstract][Hide abstract] ABSTRACT: To study the relationship between aging and the vulnerability of substantia nigra pars compacta (SNc) tyrosine hydroxylase immunoreactive positive (TH+) dopaminergic (DA) neurons. We determined the number of TH(+) DA neurons in aged rats (24 mon) compared to adult rats (5 mon) using immunohistochemistry and cell counting. Furthermore, the expression of TH mRNA and protein levels in SN was studied by semi-quantitative RT-PCR and Western blotting. A 13.6% loss of neurons was detected in rostral segment of SNc, and the expression of TH mRNA levels was also reduced (P < 0.05), however, no difference was detected in TH protein levels (P > 0.05). These data suggest that expression of TH protein may increase in the existing SNc DA neurons, which may compensate for the partial loss of TH+ DA neurons.
Preview · Article · Feb 2011 · Current Aging Science
[Show abstract][Hide abstract] ABSTRACT: We studied the relationship between aging and the vulnerability of substantia nigra pars compacta (SNc) calbindin-D-28k immunoreactive positive (CB+) dopaminergic (DA) neurons. Immunohistochemistry and cell counting were used to determine the number of CB+ DA neuron in aged rats (24 mon) compared to adult rats (5 mon). Furthermore, the expression of CB mRNA and protein levels in SN was studied by semi-quantitative RT-PCR and Western blotting. An 11% loss of CB+ DA neurons was detected in both the rostral (8.9%) and caudal (1.7%) segments but not in the intermedial segment of SNc in aged rats compared to adult rats (P<0.05). No difference was detected in CB mRNA and protein levels between aged and adult rats (P>0.05). These data suggest that expression levels of CB mRNA and protein may increase in the existing SNc DA neurons, which may compensate for the partial age dependent loss of CB+ DA neurons in the SNc.
Full-text · Article · Oct 2009 · Neuroscience Letters
[Show abstract][Hide abstract] ABSTRACT: The present study aimed to observe the morphological distribution of bone marrow (BM)-derived Nkx2-5(+) cardiac progenitor cells (CPCs) in bone marrow niche and evaluate the effect of acute myocardial ischemia (AMI) on the mobilizion of BM-derived Nkx2-5(+) CPCs. Animal models of BALB/c mouse AMI, cerebral and hind-limb ischemia were established. Nanogold labeling method, immunofluorescence and Western blot were used to identify the distribution of BM-derived Nkx2-5(+) CPCs and the expressions of Nkx2-5 protein in peripheral blood and BM after AMI. Meanwhile, in different ischemia organ models and after AMD3100 (SDF-1/CXCR4 antagonist) pretreatment in AMI model, Nkx2-5 protein expressions in peripheral blood were also assayed. Nkx2-5(+) CPCs were found to locate in cavitas medullaris. The percentage of Nkx2-5(+) CPCs in blood increased immediately after AMI. Nkx2-5 protein expression in peripheral blood was also upregulated at the timepoint of 24 h post-AMI (P<0.01) and kept stable without further enhancement from day 1 to day 7 post-AMI. In BM, Nkx2-5 protein expression was upregulated immediately after AMI and downregulated afterwards (P<0.01). After AMD3100 pretreatment in AMI group, Nkx2-5 protein expression was significantly inhibited in peripheral blood (P<0.05). In cerebral and hind-limb ischemia models, Nkx2-5 protein expressions were significantly lower than that in AMI group (P<0.01), but with no significant difference to control group. These results suggest that Nkx2-5(+) CPCs are physiologically resident in BM and AMI initiates mobilization of BM-derived Nkx2-5(+) CPCs in a predominant organ-specific manner. In the procedure of mobilization, SDF-1 may play a critical role in a chemoattracted manner.
[Show abstract][Hide abstract] ABSTRACT: In the biotherapy for tumors, microvessel permeability is the main barrier for large molecular antibody-coupled antitumor drugs to enter the tumor mass. Histamine may enrich these drugs in the tumor matrix through enhancing microvessel permeability and tissue-fluid formation. This study was to investigate whether the increased microvessel permeability and more tissue fluid formation could increase the probability of lymphatic or hemal metastasis of tumor cells.
Cultured melanoma B16 cells were inoculated into the left armpit of C57BL/6 mice to develop melanoma. Five days after inoculation, the test group were injected subcutaneously at the dorsal part with histamine (300 mg/kg) every other day for 5 times, while the control group were given normal saline. The metastasis statuses in the lymph node, liver, lung, spleen, and brain were examined by histochemistry. Student t-test and Fisher's exact test were used respectively to analyze the effects of histamine on tumor growth and metastasis.
All the mice developed melanoma after inoculation. At the end of the experiment, the tumor weight was significantly lighter in test group than in control group [(5.26 +/- 1.55) g vs. (6.96 +/- 1.31) g, P < 0.01]. The lymphatic and hemal metastasis rates were significantly lower in test group than in control group (33.3% vs. 75.0%, P < 0.05; 25.0% vs. 75.0%, P < 0.05).
Histamine can inhibit the metastasis of melanoma B16 cells in C57BL/6 mice either through lymphatic or hemal route, and this partly because of its inhibitory effect on tumor growth.
No preview · Article · Aug 2007 · Ai zheng = Aizheng = Chinese journal of cancer