Biomedical subjects

X F Wang

Publications and source records attributed to X F Wang.

At least 55 records · Page 3Linked to original sources

PubMed2000

Relationship of the livestock trade to schistosomiasis transmission in mountainous area.

OBJECTIVE: To study the relationship between the livestock trade and schistosomiasis transmission and to provide an evidence for making a strategy of schistosomiasis control in mountainous areas. METHODS: A retrospective survey and analysis was conducted to investigate the prevalence of schistosomiasis in both humans and livestock (cattle, horses, mules, donkeys and pigs), and the number and migration of livestock in Weishan County, Yunnan Province in 1980-1991. RESULTS: A positive correlation was found between the infection rate of residents and the numbers of livestock migration (R = 0.9151, P < 0.01). During 1980 to 1991 the infection rate was increased gradually along with the development of livestock husbandry, especially, from the economic reforms since 1984. In 1984 there was positive correlation in the infection rate both human and livestock (R = 0.8458, P < 0.05). The results show that the infection rates of livestock on sale including cattle, horses, mules, donkeys and pigs are 9.54%, 29.39%, 16.38%, 14.47%, 25.73% and 11.11%, respectively. CONCLUSION: The infection rate of human and livestock arises by parallel. The high frequency of livestock trade resulted in serious spreading of the infection source of schistosomiasis. The migration of the infected livestock might be an important factor in transmitting schistosomiasis.

Agricultural Workers' Diseases↗

PubMed1999

The MEK pathway is required for stimulation of p21(WAF1/CIP1) by transforming growth factor-beta.

Transforming growth factor-beta (TGF-beta)can induce the cyclin-dependent kinase inhibitors p21 and p15 in a variety of cell types. We have shown previously that Smad3 is required for the growth inhibitory activity of TGF-beta, whereas overexpression of Smads is not sufficient to activate the expression of p21 in HaCaT cells. These data suggest that an additional signaling pathway may be involved in stimulating p21 in HaCaT cells. Given the recent finding that the mitogen-activated protein kinase (MAPK) pathway can cause p21 induction and arrest cells, we examined the involvement of this pathway for p21 and p15 induction by TGF-beta. We found that TGF-beta can regulate the MAPK pathway, leading to the increased transactivation ability of transcription factor Elk. Constitutively active components in the MAPK pathway activate p21 expression, and inhibitors or dominant negative constructs for the MAPK pathway significantly decrease p21 induction by TGF-beta. Both constitutively active MEK and inhibitors for MEK have no effect on Smad activity, including DNA binding, localization, and interaction with coactivator p300/CBP. These findings suggest that the MAPK pathway may be an independent pathway that is involved in p21 and p15 induction by TGF-beta.

Benzoquinones↗

PubMed1999

Transforming growth factor-beta-mediated p15(INK4B) induction and growth inhibition in astrocytes is SMAD3-dependent and a pathway prominently altered in human glioma cell lines.

We sought to characterize the pathway by which the multifunctional cytokine transforming growth factor-beta (TGF-beta) inhibits the proliferation of normal astrocytes, and we analyzed the alterations in the TGF-beta pathway in human glioma cell lines. Upon TGF-beta treatment, primary rat astrocytes showed a significant decrease in DNA synthesis upon thymidine incorporation with a cell cycle arrest in the G(1) phase. Western analysis of the astrocytes revealed that the expression of the cyclin-dependent kinase inhibitor (CdkI) p15(INK4B) was significantly up-regulated upon TGF-beta treatment without a change in other CdkI levels. The retinoblastoma protein (Rb) became hypophosphorylated, and Cdk2 activity decreased. Analysis of Smad3 null mouse astrocytes showed a significant loss of both TGF-beta-mediated growth inhibition and p15(INK4B) induction compared with wild-type mouse astrocytes. Infection of rat astrocytes by SMAD3 and SMAD4 adenoviruses failed to induce increased expression of p15(INK4B), implying indirect transcriptional regulation of p15(INK4B) by SMAD3. High-grade human gliomas secrete TGF-beta, yet are resistant to its growth inhibitory effects. Analysis of the effects of TGF-beta on 12 human glioma cell lines showed that TGF-beta mildly inhibited the growth of six lines, had no effect on four lines, and stimulated the growth of two lines. The majority of glioma lines had homozygous deletions of the p15(INK4B) gene, except for two lines that expressed p15(INK4B) protein, which was induced further upon TGF-beta treatment. Three lines mildly induced CdkI p21(WAF1) expression in response to TGF-beta. Most tumor lines retained other TGF-beta-mediated responses, including extracellular matrix protein and angiogenic factor secretion, which may contribute to increased malignant behavior. This suggests that the loss of p15(INK4B) may explain, in part, the selective loss of growth inhibition by TGF-beta in gliomas to form a more aggressive tumor phenotype.

Animals↗

PubMed1999

Ras induces p21Cip1/Waf1 cyclin kinase inhibitor transcriptionally through Sp1-binding sites.

p21Cip1/Waf1 cyclin-dependent kinase inhibitor (p21) is inducible by Raf and mitogen-activated protein kinase kinase (MAPKK), but the level of regulation is unknown. We show here by conditional and transient Ras-expression models that Ras induces p21. Induction of p21 in conditionally Ras-expressing cells is posttranscriptional utilizing mitogen-activated protein kinase (MAPK) pathway. Transient, high-level Ras-expression induces transcriptional activation of p21 mediated by a GC-rich region in p21 promoter -83-54 bp relative to the transcription initiation site containing binding sites for Sp1-family transcription factors. Mutation of either Sp1-binding site 2 or 4 in this region decreases the magnitude of induction of promoter activity by Ras, but only the simultaneous mutation of both sites abolishes fully the induction. Electrophoretic mobility shift assays using an oligonucleotide corresponding to Sp1-binding site 2 indicate that both Sp1 and Sp3 transcription factors bind to this region. The results demonstrate that the central cytosolic growth regulator Ras is a potent transcriptional and posttranscriptional inducer of the nuclear growth inhibitor p21.

3T3 Cells↗

PubMed1999

Cooperation of Sp1 and p300 in the induction of the CDK inhibitor p21WAF1/CIP1 during NGF-mediated neuronal differentiation.

Addition of nerve growth factor (NGF) to PC12 cells promotes neuronal differentiation while inhibiting cell proliferation. In order to understand how NGF exerts its antimitogenic effect during differentiation, we have studied the mechanism by which this factor activates the promoter of the CDK inhibitor p21W4F1/CIP1. The minimal region of the p21 promoter required for the NGF-induction was mapped to a contiguous stretch of 10 bp located 83 bases upstream of the transcription initiation site. This GC-rich region was shown to interact specifically with the transcription factor Sp1 and the related protein Sp3, in either exponentially-growing or NGF-treated PC12 cells. The addition of NGF resulted in an accumulation of the transcriptional co-activator p300 in complexes associated with the NGF-responsive region. Transcriptional activity of Sp1, Sp3 and p300 was specifically induced by NGF in a Gal4-fusion assay, indicating that induction of p21 during neuronal differentiation may involve regulation of the activity of these factors by NGF. Furthermore, p300 was able to act as a co-activator for Sp1-mediated transcriptional activation in PC12 cells, suggesting that p300 and Sp1 may cooperate in activating p21 transcription during the withdrawal of neuronal precursors from the cell cycle. This hypothesis is supported by experiments showing that p300 and Sp1 form complexes in PC12 cells.

Animals↗

PubMed1999

Smads bind directly to the Jun family of AP-1 transcription factors.

Smad3 and Smad4 are sequence-specific DNA-binding factors that bind to their consensus DNA-binding sites in response to transforming growth factor beta (TGFbeta) and activate transcription. Recent evidence implicates Smad3 and Smad4 in the transcriptional activation of consensus AP-1 DNA-binding sites that do not interact with Smads directly. Here, we report that Smad3 and Smad4 can physically interact with AP-1 family members. In vitro binding studies demonstrate that both Smad3 and Smad4 bind all three Jun family members: JunB, cJun, and JunD. The Smad interacting region of JunB maps to a C-terminal 20-amino acid sequence that is partially conserved in cJun and JunD. We show that Smad3 and Smad4 also associate with an endogenous form of cJun that is rapidly phosphorylated in response to TGFbeta. Providing evidence for the importance of this interaction between Smad and Jun proteins, we demonstrate that Smad3 is required for the activation of concatamerized AP-1 sites in a reporter construct that has previously been characterized as unable to bind Smad proteins directly. Together, these data suggest that TGFbeta-mediated transcriptional activation through AP-1 sites may involve a regulated interaction between Smads and AP-1 transcription factors.

Amino Acid Sequence↗

PubMed1999

Modulation of Ca2+-dependent anion secretion by protein kinase C in normal and cystic fibrosis pancreatic duct cells.

The study investigated the role of protein kinase C (PKC) in the modulation of agonist-induced Ca2+-dependent anion secretion by pancreatic duct cells. The short-circuit current (ISC) technique was used to examine the effect of PKC activation and inhibition on subsequent ATP, angiotensin II and ionomycin-activated anion secretion by normal (CAPAN-1) and cystic fibrosis (CFPAC-1) pancreatic duct cells. The ISC responses induced by the Ca2+-mobilizing agents, which had been previously shown to be attributed to anion secretion, were enhanced in both CAPAN-1 and CFPAC-1 cells by PKC inhibitors, staurosporine, calphostin C or chelerythrine. On the contrary, a PKC activator, phorbol 12-myristate 13-acetate (PMA), was found to suppress the agonist-induced ISC in CFPAC-1 cells and the ionomycin-induced ISC in CAPAN-1 cells. An inactive form of PMA, 4alphad-phorbol 12, 13-didecanote (4alphaD), was found to exert insignificant effect on the agonist-induced ISC, indicating a specific effect of PMA. Our data suggest a role of PKC in modulating agonist-induced Ca2+-dependent anion secretion by pancreatic duct cells. Therapeutic strategy to augment Ca2+-activated anion secretion by cystic fibrosis pancreatic duct cells may be achieved by inhibition or down-regulation of PKC.

Adenosine Triphosphate↗

PubMed1999

UV radiation is a transcriptional inducer of p21(Cip1/Waf1) cyclin-kinase inhibitor in a p53-independent manner.

p53 target genes p21(Cip1/Waf1) cyclin-kinase inhibitor (p21 CKI), GADD45, bax, and cyclin G and genes affecting the redox state of the cells are implicated in p53 damage control responses. In order to attribute their functions and dependency of p53 in UV-damaged cells we undertook an analysis of UVC responses of fibroblasts derived from p53 knock-out mice. UVC radiation efficiently and rapidly inhibited DNA replication in both p53 -/- and +/+ cells. The arrest was persistent in p53 -/- fibroblasts and cells underwent apoptosis, whereas p53 +/+ cells recovered and reentered the cycle. Protein and mRNA analyses of p21 expression showed that it was induced up to sixfold with similar kinetics both in the presence and in the absence of p53. However, high doses of UV abrogated the p21 response in p53 -/- cells, whereas it was maintained in cells with normal p53. UVC radiation transcriptionally activated p21 expression as demonstrated by luciferase reporter assays using deletion constructs of the p21 promoter. The promoter assays further confirmed the independency of p53-binding sites in the activation and linked UV-responsive transcriptional regulation of p21 to two Sp1 consensus binding sites within -61 bp of the transcription initiation site. A weaker regulation was mediated by elements between -1300 to -500 bp relative to the transcription initiation site. The results suggest that in fibroblasts UVC radiation is a rapid and efficient inducer of p21 expression also in a p53-independent manner.

Animals↗

PubMed1999

Evaluation of endothelial function in hypertensive elderly patients by high-resolution ultrasonography.

BACKGROUND: Multiple investigations, both in experimental models and in middle-aged patients with essential hypertension, demonstrate impaired endothelium-dependent vasodilatation. HYPOTHESIS: We attempted to determine whether hypertension still exerts additional negative effect on endothelial function of large arteries in hypertensive elderly patients who may already be affected by endothelial dysfunction due to aging. METHODS: We compared 13 elderly patients with hypertension [69 +/- 9 years, (mean +/- standard deviation)] with 13 matched healthy elderly subjects (72 +/- 6 years) as controls. Using high-resolution vascular ultrasound, we measured brachial artery responses to reactive hyperemia (with increased flow causing endothelium-dependent dilatation) and sublingual nitroglycerin (causing endothelium-independent dilatation). RESULTS: Flow-mediated dilatation correlated inversely with age (r = -0.60, p = 0.03) in the controls. Flow-mediated dilatation was significantly impaired in hypertensive elderly patients (6.7 +/- 3.3 vs. 13.3 +/- 1.8% in controls, p < 0.0001). No significant difference could found in nitroglycerin-induced dilatation between controls (12.1 +/- 4.9%) and hypertensive elderly patients (10.2 +/- 6.8%, p = 0.5). On multivariate analysis, flow-mediated dilatation in hypertensive elderly patients was inversely related to aging (r = -0.37, p = 0.04) and mean blood pressure (r = -0.57, p = 0.03). CONCLUSIONS: Our study showed decreased flow-mediated dilatation with aging even in the healthy controls, and further decline in flow-mediated dilatation in hypertensive elderly patients compared with controls. This impairment of flow-mediated dilatation in hypertensive elderly patients was related to age and mean blood pressure, indicating that aging and hypertension may independently impair endothelial function in the brachial artery of these patients.

Aged↗

PubMed1999

Overexpression of p53 nuclear protein in premalignant and malignant laryngeal lesions.

To investigate the role of p53 nuclear protein mutations in the initiation and progression of laryngeal carcinoma, 111 premalignant and malignant laryngeal lesions (19 specimens with hyperkeratosis and 92 with carcinoma) were studied immunohistochemically. Over-expression of p53 was observed in 8 cases (42%) of laryngeal hyperkeratosis and 44 cases (47%) of laryngeal carcinoma. However, the expression of p53 showed no relationship to patients' clinical courses. Our study confirms that p53 overexpression can be found in laryngeal carcinogenesis and is an early event but not a useful prognostic marker.

Carcinoma, Squamous Cell↗

PubMed1999

Differences in responses to 70 dB clicks of cerebellar units with simple versus complex spike activity: (i) in medial and lateral ansiform lobes and flocculus; and (ii) before and after conditioning blink conditioned responses with clicks as conditioned stimuli.

Activity was recorded from 554 cerebellar units in eleven conscious cats to determine if responses to 70 dB clicks differed in units with simple and complex spike discharges. Effects of region of recording and behavioral state (with click used as a conditioned stimulus for conditioning) were also assessed. Cells with only simple spikes were distinguished from cells that had the following types of complex spike events: Type I-simple or initial spike followed > 1 ms by multiple spikes with baseline displacement (classical complex spikes), Type II--followed < or = 1 ms by spikes with or without baseline displacement (spikes in the absolute refractory period should arise from a separate site of initiation), and Type III-followed by spikes and displacement too close to the baseline noise to distinguish as Type I or II. Among the groups mean baseline activity was greatest in cells with Type I complex spikes, least in cells with Type III complex spikes, and greater in Type II cells than simple cells. Significant increases in activity within 32 ms of presenting clicks were found in the groups of Type II cells and simple cells. These appear to be the main auditory responsive cells of the cerebellar regions studied. Activity of Type II cells best reflected the temporal properties of the click; responses of simple cells had slower onsets (except in flocculus) and longer durations. Responses to click in Type II and simple cells differed in recordings from: (i) lateral ansiform lobe (lateral crus I and portions of crus II), (ii) medial ansiform lobe (medial crus I), and (iii) flocculus. The largest mean responses above baseline in the first 32 ms after click were found in Type II cells of the lateral ansiform lobe with onsets of 8-16 ms. Magnitudes of response differed before and after conditioning and backward conditioning. In the lateral ansiform lobe, the < 32 ms response to click was greater in Type II than simple cells in each state, but showed a greater increase above baseline after backward conditioning when conditioned responses were not produced than after conditioning. The onset of increased activity to click conditioned stimuli in Type II cells of the lateral ansiform region preceded the onset of the blink conditioned response after conditioning, consisted almost entirely of simple spikes, and reflected an increase in magnitude of response as opposed to an increased number of responsive units. After conditioning, an increased number of units in the flocculus responded to click conditioned stimuli in the 16-24 ms post stimulus period. Of the 16 cells with an onset of increased activity at this time, eight showed only simple spike activity. Seven of the remaining eight cells (all Type II) showed a significant increase in conditioned stimulus-evoked complex spiking above the low (usually < 1/s) baseline level of complex spike discharges. The findings support the conclusions that cerebellar units can respond rapidly enough to acoustic stimuli to play a role in auditory as well as motor processing and that the responses to 70 dB clicks differ among cells with simple and complex spike discharges. The differences are influenced substantially by the region of cerebellar recording and the behavioral state. The findings in cells of the flocculus offer the first evidence that complex as well as simple spike activity can contribute to an increased probability of discharge to click as a conditioned stimulus after conditioning.

Acoustic Stimulation↗

PubMed1999

Effects of astrocytes on neuronal attachment and survival shown in a serum-free co-culture system.

In order to study the neurosupportive effects of glial cells, we optimized a glial-neuron non-contact co-culture method. Astrocyte conditioned medium (ACM) and an astrocyte feeder layer were used to promote neuronal attachment and neuronal survival respectively. Neuron-enriched cultures were prepared from cortices of E-18 day rat embryos. Instead of plating cells in serum-supplemented medium, as an indispensable first-step procedure for many serum-free culture protocols, we found that coating the coverslips briefly with ACM was sufficient for the healthy attachment and neurite outgrowth of the dissociated neurons in serum-free medium. A high survival rate of the low density (4x10(4) cells/cm(2)) neuronal cultures was achieved by co-culturing primary neurons with an astrocyte feeder layer. This non-contact co-culture method could be easily implemented with ordinary culture dishes. Our serum-free chemically defined medium was MEM supplemented with insulin, transferrin, selenium and pyruvate. In this serum-free medium, glial cells did not proliferate and a neuron-enriched population was obtained without the need for mitotic inhibitors. Our experimental results reveal a critical role for astrocytes in neuronal attachment and growth. This method can be used to study glial-neuron interactions as well as culturing low-density population of pure neurons.

Animals↗

PubMed1999

Smad3-Smad4 and AP-1 complexes synergize in transcriptional activation of the c-Jun promoter by transforming growth factor beta.

Transcriptional regulation by transforming growth factor beta (TGF-beta) is a complex process which is likely to involve cross talk between different DNA responsive elements and transcription factors to achieve maximal promoter activation and specificity. Here, we describe a concurrent requirement for two discrete responsive elements in the regulation of the c-Jun promoter, one a binding site for a Smad3-Smad4 complex and the other an AP-1 binding site. The two elements are located 120 bp apart in the proximal c-Jun promoter, and each was able to independently bind its corresponding transcription factor complex. The effects of independently mutating each of these elements were nonadditive; disruption of either sequence resulted in complete or severe reductions in TGF-beta responsiveness. This simultaneous requirement for two distinct and independent DNA binding elements suggests that Smad and AP-1 complexes function synergistically to mediate TGF-beta-induced transcriptional activation of the c-Jun promoter.

Amino Acid Sequence↗

PubMed1999

Targeted disruption of Smad3 reveals an essential role in transforming growth factor beta-mediated signal transduction.

The Smads are a family of nine related proteins which function as signaling intermediates for the transforming growth factor beta (TGF-beta) superfamily of ligands. To discern the in vivo functions of one of these Smads, Smad3, we generated mice harboring a targeted disruption of this gene. Smad3 null mice, although smaller than wild-type littermates, are viable, survive to adulthood, and exhibit an early phenotype of forelimb malformation. To study the cellular functions of Smad3, we generated Smad3 null mouse embryonic fibroblasts (MEFs) and dermal fibroblasts. We demonstrate that null MEFs have lost the ability to form Smad-containing DNA binding complexes and are unable to induce transcription from the TGF-beta-responsive promoter construct, p3TP-lux. Using the primary dermal fibroblasts, we also demonstrate that Smad3 is integral for induction of endogenous plasminogen activator inhibitor 1. We subsequently demonstrate that Smad3 null MEFs are partially resistant to TGF-beta's antiproliferative effect, thus firmly establishing a role for Smad3 in TGF-beta-mediated growth inhibition. We next examined cells in which Smad3 is most highly expressed, specifically cells of immune origin. Although no specific developmental defect was detected in the immune system of the Smad3 null mice, a functional defect was observed in the ability of TGF-beta to inhibit the proliferation of splenocytes activated by specific stimuli. In addition, primary splenocytes display defects in TGF-beta-mediated repression of cytokine production. These data, taken together, establish a role for Smad3 in mediating the antiproliferative effects of TGF-beta and implicate Smad3 as a potential effector for TGF-beta in modulating immune system function.

Animals↗

PubMed1999

c-Jun enhancement of cyclic adenosine 3',5'-monophosphate response element-dependent transcription induced by transforming growth factor-beta is independent of c-Jun binding to DNA.

Transforming growth factor-beta (TGFbeta) enhances transcription from reporter genes regulated by a single consensus cAMP-response element (CRE) upon transfection into the immortalized human keratinocyte cell line, HaCaT. Whereas both CRE-binding protein (CREB) and c-Jun present in extracts of unstimulated cells can complex with a CRE in gel-shift experiments, TGFbeta treatment increases the amount of c-Jun found in the complex. Overexpression of c-Jun is sufficient to increase CRE and GAL4-CREB-dependent transcription and mimics the stimulatory effects of TGFbeta on transcription from either reporter gene. Surprisingly, although a portion of CREB in unstimulated cells is phosphorylated on the activating serine residue, Ser-133, this level of phospho-CREB is not altered by TGFbeta treatment. In fact, the CREB-dependent transcriptional effects of TGFbeta or c-Jun do not require phosphorylation of Ser-133, although CREB-binding protein (CBP) is required as evidenced by the observation that the adenoviral oncoprotein E1A can block the effects of both agents. c-Jun enhancement of CRE or GAL4-CREB-dependent transcription neither requires the DNA-binding nor N-terminal domains of c-Jun. Collectively, these results are consistent with a model in which signaling pathways initiated by TGFbeta can stimulate CREB-dependent transcription by increasing the cellular concentration of c-Jun, which participates in activation of the CBP-containing transcription complex.

Adenovirus E1A Proteins↗

PubMed1999

Studies on plasma endothelin changes in varicocele patients.

AIM: To investigate the possible role endothelin may play in the pathogenesis of varicocele and varicocele-induced infertility. METHODS: In varicocele patients, radioimmunoassay is used to determine the blood endothelin concentration in the spermatic vein and the antecubital vein separately. RESULTS: The blood endothelin concentration of the spermatic vein (66.8 +/- 23.5 pg/mL) was significantly higher (P < 0.05) than that of the antecubital vein (55.3 +/- 25.3 pg/mL). The endothelin concentration in the spermatic vein in Grade II varicocele patients was not significantly different from that in Grade III patients (P = 0.87). CONCLUSION: The higher blood endothelin level in the spermatic vein may indicate the involvement of endothelin in the pathophysiology of varicocele and varicocele-induced infertility.

Adult↗

PubMed1998

The effect of ACPD on the responses to NMDA and AMPA varies with layer in slices of rat visual cortex.

The effect of 1S,3R-aminocyclopentane dicarboxylic acid (ACPD) was measured on cells from various layers in slices of the rat visual cortex using whole-cell recording techniques. The position of the recorded cell was estimated by distance from pia to the layer VI/white matter boundary, and verified in 34/97 cells by staining with biocytin. Potentiation or depression of the responses to NMDA and AMPA by the metabotropic glutamate agonist ACPD was examined by iontophoresis of the drugs close to the cell body. Iontophoresis of ACPD had different effects in different layers. In layer VI, ACPD produced a substantial depolarization, which augmented the responses to NMDA and AMPA. In layer V, ACPD did not produce a significant depolarization, but potentiated the response to NMDA and AMPA. In layer IV, ACPD produced a small hyperpolarization, and depressed the response to NMDA. In layers II and III, the results were small and variable. Most recordings from stained cells were from pyramidal cells. Where recordings from non-pyramidal cells were obtained (3/34), results were the same as from pyramidal cells in the same layer. The same results were obtained when tetrodotoxin was in the bath solution. We conclude that the potentiation or depression of the response to NMDA and AMPA by ACPD varies with layer in rat visual cortex.

Animals↗

PubMed1998

Functional expression of a Ca2+-activated K+ channel in Xenopus oocytes injected with RNAs from the rat testis.

The present study investigated the feasibility of using Xenopus oocytes to express sperm ion channel by injection of RNAs extracted from the rat testis. The RNA-injected oocytes expressed an outwardly rectifying current which was dependent on K+ concentration and inhibitable by K+ channel blockers, charybdotoxin (CTX) and tetraethylammonium (TEA). The Ca2+ ionophore, ionomycin, could also stimulate current activation with similar current characteristics in the RNA-injected oocytes, suggesting the expression of a Ca2+-activated K+ channel. Immunolocalization indicated predominant Ca2+-activated K+ channel immunoreactivity associated with spermatogenic cells. Reverse transcriptase-polymerase chain reaction studies confirmed the expression of the Ca2+-activated K+ channel mRNA in isolated spermatogenic cells. Our results suggest that ion channels and/or receptors of spermatogenic cells could be investigated using the Xenopus oocyte as an expression system. The present study also suggests that sperm may possess a Ca2+-activated K+ channel which has been implicated in the process of sperm activation and gamete interaction.

Animals↗