Biomedical subjects

Phil-Ok Koh

Publications and source records attributed to Phil-Ok Koh.

8 recordsLinked to original sources

PubMed2006

Ethanol exposure decreases cell proliferation and increases apoptosis in rat testes.

Ethanol exposure is known to suppress male reproductive activity in laboratory animals and humans. The present study was designed to evaluate whether chronic ethanol exposure decreases proliferative activity or increases apoptosis in the testes. Ethanol (1.5 g/kg or 3 g/kg i.p., 15% v/v in saline) was administrated to adult male rats for 10 days. Proliferating cell nuclear antigen (PCNA) was used as a proliferative marker. Western blot analysis showed that ethanol administration significantly reduced the level of PCNA. Also, immunoreactivity of PCNA-positive cells in the spermatogonia and primary spermatocytes were decreased by ethanol exposure. However, the number of TUNEL-positive cells was significantly increased in the testicular germ cells of ethanol-treated rats. Moreover, ethanol administration significantly increased the level of activated caspase-3 in testes. In conclusion, our findings suggest that ethanol may partly contribute to the suppression of male reproductive activity through a reduction of cell proliferation and an enhancement of cell death in rat testes.

Animals↗

PubMed2006

17beta-estradiol pretreatment prevents the global ischemic injury-induced decrease of Akt activation and bad phosphorylation in gerbils.

Estradiol acts as a neuroprotective factor against ischemic brain injury. This study investigated whether estradiol modulates neuroprotective mechanism through the activation of Akt and its downstream target such as Bad in global ischemic injury. Adult female gerbils were ovariectomized and treated with estradiol prior to ischemic injury. Transient cerebral ischemia was accomplished by bilateral clipping of the common carotid artery for 5 min. Brains were collected on 1, 3, 5 day after injury. In hippocampal CA1 region of non-treated gerbils, most of neuronal cells exhibited pyknotic nuclei and showed the positive reaction of TUNEL staining on 5 day after injury. However, estradiol significantly reduced the neuronal cell death. Potential activation was measured by phosphorylation of Akt at Ser473 and Bad at Ser136 using western blot analysis. The levels of pAkt and pBad were significantly decreased in non-treated gerbils on 1-5 day after injury. However, estradiol prevents the global ischemic injury-induced decrease of pAkt and pBad. Our findings suggest that estradiol prevents cell death due to global ischemic injury and that Akt activation and Bad phosphorylation by estradiol mediated these protective effects.

Animals↗

PubMed2006

Estrogen modulates Bcl-2 family proteins in ischemic brain injury.

Estradiol acts as a neuroprotective factor against brain injury. This study investigated whether estradiol modulates the Bcl-2 family proteins in ischemic brain injury. Adult female rats were ovariectomized and treated with estradiol prior to middle cerebral artery occlusion (MCAO). Brains were collected 24 hr after MCAO, and infarct volumes were analyzed. Estradiol significantly reduces the infarct volume and decreases the positive cells of TUNEL staining in cerebral cortex. In ischemic cerebral cortex, the level of Bcl-2 was decreased, and the level of Bax was significantly increased. Estradiol prevents the injury-induced decrease of Bcl-2 and increase of Bax. In conclusion, our findings suggest that estradiol plays a potent protective role in brain injury through the regulation of Bcl-2 family proteins.

Animals↗

PubMed2006

Decrease of pituitary adenylate cyclase activating polypeptide and its type I receptor mRNAs in rat testes by ethanol exposure.

The present study was designed to evaluate the effect of ethanol on pituitary adenylate cyclase activating polypeptide (PACAP) and its typ I (PAC1) receptor expression in adult rat testes. Ethanol (3 g/kg i.p., 15% v/v in saline) was administrated to adult male rats for 10 days. Using northern blot analysis, the present study showed the reduction of PACAP mRNA levels in rat testes by ethanol administration. Also, ethanol decreased the expression level of PAC1 receptor in testes. In particular, in situ hybridization clearly showed the decrease of PAC1 receptor mRNA expression in Leydig cells, which produce testosterone. Furthermore, the serum level of testosterone was significantly decreased in the ethanol-treated group. In conclusion, our findings suggest that the decrease of PACAP and PAC1 receptor expression in rat testes by ethanol exposure may partly contribute to the suppression of male reproductive activity.

Animals↗

PubMed2006

Ethanol decreases the expression of pituitary adenylate cyclase activating polypeptide in rat testes.

The present study was designed to evaluate the effect of ethanol on pituitary adenylate cyclase activating polypeptide (PACAP) expression in adult rat testes. Ethanol (3 g/kg i.p., 15% v/v in saline) was administrated to adult male rats for 10 days. Using northern blot analysis, we elucidated the decrease of PACAP mRNA in rat testes by ethanol administration. The level of PACAP mRNA was decreased by 46.5% in testes of the ethanol-treated animals, compared to that of saline-treated animals. In particular, ethanol exposure decreased the expression of PACAP mRNA and protein in developing germ cells, which are sperm cell progenitors. Thus, our findings suggest that the decrease of PACAP in developing germ cells by ethanol administration may contribute to the suppression of male reproductive activity.

Animals↗

PubMed2005

The effect of thrombin on astrocyte stellation with regional specificity.

In this study, we have examined the possible existence of astrocyte regional heterogeneity in thrombin effect on astrocyte stellation. Neonatal astrocytes were cultured for 2 weeks from six different regions of the neonatal rat brain, including the cerebral cortex, hippocampus, brainstem, midbrain, hypothalamus and cerebellum. Culture medium was changed to DMEM containing 8-CPT-cyclic AMP (cAMP) or isoproterenol plus various concentrations of thrombin for 2 hr. Thrombin effectively blocked both cAMP- and isoproterenol-induced cell stellation in a dose-dependent manner in all regional astrocytes except cerebellar astrocytes. RT-PCR analysis showed that thrombin receptor mRNA was expressed in all regional astrocytes, suggesting that cerebellar astrocytes may maintain a unique signaling pathway downstream of the thrombin receptor.

Animals↗

PubMed2005

Expression of pituitary adenylate cyclase activating polypeptide and its type I receptor mRNAs in human placenta.

Pituitary adenylate cyclase activating polypeptide (PACAP) was first isolated from ovine hypothalamus and was known to stimulate the release of growth factor in various cells. Recently, we reported the cellular localization of PACAP and its type I (PAC1) receptor in rat placenta during pregnancy. Placenta is a critical organ that synthesizes several growth factors and angiogenic factors for the fetal development and its own growth. However, there is little information regarding the cellular localization of PACAP and its receptor in human placenta at various gestations. The aim of the present study was to define the expression and distribution of PACAP and PAC1 receptor mRNAs in the human placenta during the pregnancy period. PACAP and PAC1 receptor mRNAs were expressed in stroma cells of stem villi and terminal villi. At the early stage, on 7 and 14 weeks, PACAP and PAC1 receptor genes were moderately expressed in stroma cells surrounding the blood vessels within stem villi. These genes were strongly expressed in stroma cells of stem villi and terminal villi on 24 and 38 weeks. The expression of these genes was increased as gestation advanced, and localized in the same areas. Localization of PACAP and PAC1 receptor demonstrate the evidence that PACAP may play an important role, as an autoregulator or pararegulator via its PAC1 receptor. In conclusion, our findings strongly suggest that PACAP may have a critical role in physiological function of the placenta for gestational maintenance and fetal growth.

Chorionic Villi↗

PubMed2003

D1 dopamine receptors in the mouse prefrontal cortex: Immunocytochemical and cognitive neuropharmacological analyses.

Dopamine D1 receptors have critical neuromodulatory influences on the working memory functions of the prefrontal cortex, a brain region affected in many neuropsychiatric disorders. When D1 receptor agents are administered to rats or monkeys performing working memory tasks, an "inverted U" dose/response function is typically observed, whereby either too little or too much D1 receptor stimulation impairs working memory. There are two subtypes of D1 receptors, the D1A and the D1B (also known as the D1 and D5, respectively), but the relative contributions of these subtypes to prefrontal cortical function are not known, as there are no pharmacological agents that can distinguish between these receptors. Thus, genetically altered mice are needed to address this question. However, it is not known whether the mouse prefrontal cortex contains both D1A and D1B receptor subtypes, nor is it known whether mice will exhibit responses to D1 receptor agonists similar to those seen in rats and monkeys. The current study examined these issues by immunostaining the mouse brain with specific antibodies directed at the D1A and D1B receptor subtypes and by assessing the effects of increasing doses of a D1 receptor agonist, SKF81297, on spatial working memory performance in mice. Results indicate that mice are generally similar to monkeys and rats, expressing both D1A and D1B receptors in the prefrontal cortex and exhibiting an inverted "U" dose/response curve when administered SKF81297.

Animals↗