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Biomedical subjects

J He

Publications and source records attributed to J He.

At least 181 records · Page 10Linked to original sources
PubMed2000

[Progress in charge-coupled device and its applications].

Charge-coupled device (CCD) is a photosensitive element based on the metal-oxidesemiconductor technology. Currently, it has a number of benefits; broad spectral range response, low detection limit, wide dynamic range, minimal dark current and readout noise as well as abilities of signal integration, simultaneous multichannel detection and real-time detection. In this paper, the operational principle, features and performance characterization of CCD are introduced and its applicaton in spectral detection and spectral imaging are veiwed. The development of CCD technique has brought a revolutionary progress in the spectroscopic areas. Its future developments are also outlooked.

Electrochemistry↗
PubMed1999

Cocaine and apoptosis in myocardial cells.

Toxic effects of cocaine on the heart muscle have been known for many years. Cardiovascular complications related to cocaine abuse include myocardial ischemia and infarction, inflammation, and disease of the heart muscle, rhythm disturbances, and sudden cardiac death. Cocaine toxicity-related cardiac morbidity and mortality are often due to several interacting mechanisms. Cocaine also has a potent pharmacological effect, indirectly stimulating the sympathetic nervous system, and it has a direct toxic effect on the heart. Although apoptosis (also called programmed cell death) has been shown to play an important role in the pathogenesis of several diseases in the heart, including heart failure and ischemic myocardial infarction, the role of apoptosis in the toxic effect of cocaine on the heart has not been explored. Recent studies indicated that cocaine causes apoptotic cell death in both adult and fetal heart muscles. Increased oxidative stress and reactive oxygen species, and the subsequent activation of a "stress responsive" enzyme (p38-mitogen-activated protein kinase) in the heart may play an important role in cocaine-induced apoptosis in the heart muscle. These findings suggest a new way to understand the cardiotoxic effects of cocaine, and may have potential clinical implications in the better management of cocaine-induced heart diseases. Anat Rec (New Anat): 257:208-216, 1999.

Animals↗
PubMed1999

Dietary sodium intake and subsequent risk of cardiovascular disease in overweight adults.

CONTEXT: Dietary sodium is positively associated with blood pressure, and ecological and animal studies both have suggested that high dietary sodium intake increases stroke mortality. OBJECTIVE: To examine the risk of cardiovascular disease associated with dietary sodium intake in overweight and nonoverweight persons. DESIGN: Prospective cohort study. SETTING: The first National Health and Nutrition Examination Survey Epidemiologic Follow-up Study, conducted in 1982-1984, 1986, 1987, and 1992. PARTICIPANTS: Of those aged 25 to 74 years when the survey was conducted in 1971 -1975 (14407 participants), a total of 2688 overweight and 6797 nonoverweight persons were included in the analysis. MAIN OUTCOME MEASURES: Dietary sodium and energy intake were estimated at baseline using a single 24-hour dietary recall method. Incidence and mortality data for cardiovascular disease were obtained from medical records and death certificates. RESULTS: For overweight and nonoverweight persons, over an average of 19 years of follow-up, the total number of documented cases were as follows: 680 stroke events (210 fatal), 1727 coronary heart disease events (614 fatal), 895 cardiovascular disease deaths, and 2486 deaths from all causes. Among overweight persons with an average energy intake of 7452 kJ, a 100 mmol higher sodium intake was associated with a 32% increase (relative risk [RR], 1.32; 95% confidence interval [CI], 1.07-1.64; P = .01) in stroke incidence, 89% increase (RR, 1.89; 95% CI, 1.31-2.74; P<.001) in stroke mortality, 44% increase (RR, 1.44; 95% CI, 1.14-1.81; P = .002) in coronary heart disease mortality, 61% increase (RR, 1.61; 95% CI, 1.32-1.96; P<.001) in cardiovascular disease mortality, and 39% increase (RR, 1.39; 95% CI, 1.23-1.58; P<.001) in mortality from all causes. Dietary sodium intake was not significantly associated with cardiovascular disease risk in nonoverweight persons. CONCLUSIONS: Our analysis indicates that high sodium intake is strongly and independently associated with an increased risk of cardiovascular disease and all-cause mortality in overweight persons.

Adult↗
PubMed1999

[The feature of influenza virus activity and genetic characterization of HA1 gene of influenza A H3N2 viruses isolated from 1994-1997 in Shenzhen].

OBJECTIVE: To understand the feature of influenza virus activity and genetic characterization of HA1 gene of influenza A H3N2 viruses isolated in recently years in Shenzhen. METHODS: The specimens were inoculated into amniotic and allantoic cavities of the embryonated chicken eggs for viral isolation. The isolates were typed with HI test. Virion RNA extracted from allantoic fluid by Rneasy RNA extraction kit was used for RT-PCR amplification. Afterward, the product of PCR was purified with purification kit. RNA sequence analysis was performed by Sanger dideoxy-mediated nucleotide chain termination method. RESULTS: Influenza A H3N2, H1N1 and B viruses were cocirculating in men in Shenzhen in recent years. However, the extent of their activities was not the same in a single year. The influenza B virus was the predominant strain in 1994 and 1997, but the predominant strain was H3N2 virus in 1996. The genetic analysis showed that the substitution of amino acids occured year by year and was mainly located at antigenic determinants or receptor binding site on HA1 domain of H3N2 viruses. CONCLUSION: Influenza A H3N2, H1N1 and B viruses were still co-circulating in men in Shenzhen in recent years, the predominant strain of influenza virus was different in different years. An increase of influenza A H3N2 virus activity in 1996 was due to the substitution of amino acids sequences on viral HA1 domain.

Amino Acid Sequence↗
PubMed1999

Etk/Bmx, a PH-domain containing tyrosine kinase, protects prostate cancer cells from apoptosis induced by photodynamic therapy or thapsigargin.

Prostate carcinoma (PCA) is the most frequently diagnosed malignancy in American men. PCA at advanced stages can both proliferate abnormally and resist apoptosis. Among the many known signal transduction pathways, phosphatidylinositide-3'OH kinase (PI3-kinase) has been shown to play an important role in cell survival and resistance to apoptosis. In this study, we investigate the involvement of Etk/Bmx, a newly discovered tyrosine kinase that is a substrate of PI3-kinase, in protection of prostate cancer cells from apoptosis. Parental LNCaP cells and two derivative cell lines, one overexpressing wild type Etk (Etkwt) and the other expressing a dominant negative Etk (EtkDN), were used to study the function of Etk. The cells were treated with photodynamic therapy (PDT), a newly approved cancer treatment which employs a photosensitizer and visible light to produce an oxidative stress in cells, often leading to apoptosis. Our results indicate that PDT induces apoptosis in LNCaP cells, as measured by DNA fragmentation and by cleavage of poly(ADP-ribose) polymerase (PARP), and moreover, the extent of apoptosis was much reduced in Etkwt cells as compared to LNCaP or EtkDN cells. Assay of overall cell viability confirmed that Etkwt cells were considerably less sensitive to PDT than were the parental LNCaP or EtkDN cells. Similar results were found in response to thapsigargin (TG). A specific inhibitor of PI3-kinase, LY294002, abolished Etk activity and markedly increased TG-induced PARP cleavage. The results suggest that Etk/Bmx is an efficient effector of PI3-kinase and that the newly described PI3-kinase/Etk pathway is involved in the protection of prostate carcinoma cells from apoptosis in response to PDT or TG.

Apoptosis↗
PubMed1999

Passive smoking and the risk of coronary heart disease--a meta-analysis of epidemiologic studies.

BACKGROUND: The effect of passive smoking on the risk of coronary heart disease is controversial. We conducted a meta-analysis of the risk of coronary heart disease associated with passive smoking among nonsmokers. METHODS: We searched the Medline and Dissertation Abstracts Online data bases and reviewed citations in relevant articles to identify 18 epidemiologic (10 cohort and 8 case-control) studies that met prestated inclusion criteria. Information on the designs of the studies, the characteristics of the study subjects, exposure and outcome measures, control for potential confounding factors, and risk estimates was abstracted independently by three investigators using a standardized protocol. RESULTS: Overall, nonsmokers exposed to environmental smoke had a relative risk of coronary heart disease of 1.25 (95 percent confidence interval, 1.17 to 1.32) as compared with nonsmokers not exposed to smoke. Passive smoking was consistently associated with an increased relative risk of coronary heart disease in cohort studies (relative risk, 1.21; 95 percent confidence interval, 1.14 to 1.30), in case-control studies (relative risk, 1.51; 95 percent confidence interval, 1.26 to 1.81), in men (relative risk, 1.22; 95 percent confidence interval, 1.10 to 1.35), in women (relative risk, 1.24; 95 percent confidence interval, 1.15 to 1.34), and in those exposed to smoking at home (relative risk, 1.17; 95 percent confidence interval, 1.11 to 1.24) or in the workplace (relative risk, 1.11; 95 percent confidence interval, 1.00 to 1.23). A significant dose-response relation was identified, with respective relative risks of 1.23 and 1.31 for nonsmokers who were exposed to the smoke of 1 to 19 cigarettes per day and those who were exposed to the smoke of 20 or more cigarettes per day, as compared with nonsmokers not exposed to smoke (P=0.006 for linear trend). CONCLUSIONS: Passive smoking is associated with a small increase in the risk of coronary heart disease. Given the high prevalence of cigarette smoking, the public health consequences of passive smoking with regard to coronary heart disease may be important.

Coronary Disease↗
PubMed1999

Plasma insulin levels and incidence of hypertension in African Americans and whites.

BACKGROUND: Hyperinsulinemia may play an important role in the pathogenesis of hypertension in whites but the role of hyperinsulinemia in hypertension in African Americans is controversial. SUBJECTS AND METHODS: We studied the relationship between insulin levels and subsequent incidence of hypertension in 140 African Americans and 237 whites who were initially screened for possible participation in the Trials of Hypertension Prevention, phase 1. Plasma insulin and serum glucose were measured at baseline and at a follow-up examination 7 years later. Blood pressure was measured by trained observers using a random-zero sphygmomanometer. Incident hypertension was defined as an average systolic pressure of 160 mm Hg or higher and/or diastolic pressure of 95 mm Hg or higher at a single visit and/or use of antihypertensive medication during follow-up. RESULTS: Over the 7 years of follow-up, the incidence of hypertension was 25.7% in the African Americans and 25.3% in the whites. Baseline plasma insulin and insulin-to-glucose ratio were associated with an increased risk of hypertension in both the African Americans and the whites. After adjustment for age, sex, race, body mass, heart rate, and alcohol consumption at baseline as well as intervention assignment in the Trials of Hypertension Prevention, phase 1, a 1-SD (21 pmol/mmol) difference in baseline insulin-to-glucose ratio was associated with a 2.77 (95% confidence interval, 1.48-5.19) odds ratio of hypertension in the African Americans and a 1.69 (95% confidence interval, 1.08-2.64) odds ratio in the whites. CONCLUSION: These results suggest that higher plasma insulin levels are associated with an increased risk of hypertension in both African Americans and whites.

Adult↗
PubMed1999

Thrombopoietin-induced conformational change in p53 lies downstream of the p44/p42 mitogen activated protein kinase cascade in the human growth factor-dependent cell line M07e.

Thrombopoietin is a cytokine with potent megakaryocytopoietic and thrombopoietic activities in vivo. Wild-type p53 is a conformationally flexible, anti-oncogenic transcription factor that plays a principal role in mediating growth factor withdrawal-induced apoptosis in factor-dependent hematopoietic cells. We recently reported that Tpo induces a conformational change in and functional inactivation of p53, coincident with its anti-apoptotic effects, in the human factor-dependent cell line M07e. In an effort to identify potential signaling cascades through which Tpo illicits these effects on p53, we report here that treating M07e cells with MAPK kinase inhibitor PD98059 dramatically suppressed Tpo-induced conformational change in p53 as well as Tpo-enhanced viability in M07e cells in a p53-dependent manner. Furthermore, the expression of constitutively active Raf1 in M07e cells induced conformational change in p53 independent of Tpo stimulation. Inhibition of the JAK/STAT pathway revealed that JAK/STAT signaling plays an insignificant role in conformational modulation of p53 and apoptosis suppression. Inhibition of phosphatidylinositol-3 kinase did not have a significant effect on p53 conformation but did have a weak but significant effect on Tpo-enhanced viability. Cytokine-induced activation of the MAPK pathway and the subsequent functional neutralization of p53, may be an event by which apoptosis is commonly suppressed in hematopoiesis.

Animals↗
PubMed1999

Cholera toxin suppresses interleukin (IL)-12 production and IL-12 receptor beta1 and beta2 chain expression.

Cholera toxin (CT) is a potent mucosal vaccine adjuvant, which has been shown to induce T helper cell type 2 (Th2) responses in systemic and mucosal tissues. We report that CT inhibits the production of interleukin (IL)-12, a major Th2 counterregulatory cytokine. IL-12 p70 production by stimulated human monocytes was inhibited by CT in a dose-dependent manner. This suppression occurred at the level of gene transcription, was maximal at low concentrations of CT, and was dependent on the A subunit of the toxin, since purified CT B subunit had minimal effect. CT also inhibited the production of IL-12 p70 by monocyte-derived dendritic cells, as well as the production of tumor necrosis factor alpha, but not IL-10, IL-6, or transforming growth factor (TGF)-beta1, by stimulated monocytes. The effects of CT were not due to autocrine production of IL-10, TGF-beta1, or prostaglandin E2. CT inhibited the production of IFN-gamma by anti-CD3-stimulated human peripheral blood mononuclear cell, due in part to suppression of IL-12 production, but also to the inhibition of expression of the beta1 and beta2 chains of the IL-12 receptor on T cells. In vivo, mice given CT before systemic challenge with lipopolysaccharide had markedly reduced serum levels of IL-12 p40 and interferon gamma. These data demonstrate two novel mechanisms by which CT can inhibit Th1 immune responses, and help explain the ability of mucosally administered CT to enhance Th2-dependent immune responses.

Adjuvants, Immunologic↗
PubMed1999

Faithful expression of green fluorescent protein (GFP) in transgenic zebrafish embryos under control of zebrafish gene promoters.

Although the zebrafish has become a popular model organism for vertebrate developmental and genetic analyses, its use in transgenic studies still suffers from the scarcity of homologous gene promoters. In the present study, three different zebrafish cDNA clones were isolated and sequenced completely, and their expression patterns were characterized by whole-mount in situ hybridization as well as by Northern blot hybridization. The first clone encodes a type II cytokeratin (CK), which is specifically expressed in skin epithelia in early embryos and prominently expressed in the adult skin tissue. The second clone is muscle specific and encodes a muscle creatine kinase (MCK). The third clone, expressed ubiquitously in all tissues, is derived from an acidic ribosomal phosphoprotein P0 (arp) gene. In order to test the fidelity of zebrafish embryos in transgenic expression, the promoters of the three genes were isolated using a rapid linker-mediated PCR approach and subsequently ligated to a modified green fluorescent protein (gfp) reporter gene. When the three hybrid GFP constructs were introduced into zebrafish embryos by microinjection, the three promoters were activated faithfully in developing zebrafish embryos. The 2.2-kb ck promoter was sufficient to direct GFP expression in skin epithelia, although a weak expression in muscle was also observed in a few embryos. This pattern of transgenic expression is consistent with the expression pattern of the endogenous cytokeratin gene. The 1.5-kb mck promoter/gfp was expressed exclusively in skeletal muscles and not elsewhere. By contrast, the 0.8-kb ubiquitous promoter plus the first intron of the arp gene were capable of expressing GFP in a variety of tissues, including the skin, muscle, lens, neurons, notochord, and circulating blood cells. Our experiments, therefore, further demonstrated that zebrafish embryos can faithfully express exogenously introduced genes under the control of zebrafish promoters.

Animals↗
PubMed1999

Germline mutations of p53 but not p16/CDKN2 or PTEN/MMAC1 tumor suppressor genes predispose to gliomas. The ANOCEF Group. Association des NeuroOncologues d'Expression Française.

Constitutional DNA from 44 selected patients suspected of being genetically predisposed to develop astrocytic tumors was analyzed for germline mutations of the p53, p16, and PTEN genes. Six constitutional missense mutations of the p53 gene were identified (13.6%), but no mutations of the p16 and PTEN genes were found, suggesting that (1) germline p53 mutations contribute to a small portion of astrocytic tumors, (2) inherited mutations of the p16 and PTEN gene do not predispose to the development of gliomas, and (3) other genes are involved in glioma predisposition.

Amino Acid Substitution↗
PubMed1999

Sport-caught fish consumption and conception delay in licensed Michigan anglers.

Between 1993 and 1995, we surveyed 4931 licensed anglers aged 17-34 years residing in 10 Michigan counties bordering a Great Lake. Responses were received from 1443 anglers and 844 of their partners. Lifetime sport-caught fish consumption was estimated as the number of sport-caught fish meals consumed in the previous 12 months times years since 1970 in which sport-caught fish were consumed. Analysis was restricted to currently married couples (n=626). Lifetime sport-caught fish consumption was categorized in men as 0 (14%); 1-114 (27%); 115-270 (30%); 271-1127 (29%) meals; and in women as 0 (28%); 1-54 (26%); 55-138 (27%); fand 139-1127 (19%) meals, respectively. Conception delay (ever having failed to conceive after 12 months of trying) was reported by 13% of both men and women. Among men, the unadjusted odds ratios (OR) for conception delay were 1.2, 1.3, and 2.0 across the three increasing levels of sport-caught fish consumption compared to none (trend test P=0.06). After adjustment for age, race, region of Michigan, household income, educational attainment, smoking, alcohol consumption, and partner's sport fish consumption, the OR for conception delay in men were 1.4, 1.8, and 2.8, respectively. In women, unadjusted OR for conception delay were 0.9, 1.0, and 1.4 with increasing sport-caught fish consumption (trend test P=0.35). With the same covariates and the sport-caught fish consumption of the woman's partner included in the model, the OR were 0.8, 0.8, and 1.0, respectively. These data suggest a modest association, in men only, of sport-caught fish consumption with risk of conception delay.

Adolescent↗
PubMed1999

Elevated systolic blood pressure and risk of cardiovascular and renal disease: overview of evidence from observational epidemiologic studies and randomized controlled trials.

The effect of elevated blood pressure on risk of cardiovascular and renal disease has been documented in both observational epidemiologic studies and clinical trials. However, these studies have traditionally concentrated on diastolic blood pressure to characterize the risk associated with hypertension. We reviewed evidence from prospective studies and randomized controlled trials to quantify the risk associated with systolic blood pressure. Prospective studies and randomized controlled clinical trials that were published in English-language journals were retrieved using MEDLINE, bibliographies, and the authors' reference files. All retrieved publications were reviewed and information on sample size, duration, study design, antihypertensive medication, participant characteristics, and outcomes was abstracted for randomized controlled trials that reported systolic blood pressure reduction during intervention. Several prospective studies indicate that the association between systolic blood pressure and risk of coronary heart disease, stroke, and end-stage renal disease is continuous, graded, and independent. Furthermore, they suggest that the association of systolic blood pressure with these outcomes is stronger than that of diastolic blood pressure. Pooling of the data available from randomized controlled trials indicates that an average reduction of 12 to 13 mm Hg in systolic blood pressure over 4 years of follow-up is associated with a 21% reduction in coronary heart disease, 37% reduction in stroke, 25% reduction in total cardiovascular mortality, and 13% reduction in all-cause mortality rates. These data indicate that systolic blood pressure is an independent and strong predictor for risk of cardiovascular and renal disease.

Blood Pressure↗
PubMed1999

Antiserum generated by DNA vaccine binds to hepatitis E virus (HEV) as determined by PCR and immune electron microscopy (IEM): application for HEV detection by affinity-capture RT-PCR.

Previously, we have described that injection of an expression vector containing hepatitis E virus (HEV) open reading frame 2 (HEV-ORF-2) generated a strong antibody response in mice. To characterize the reaction of this antiserum with native HEV and to evaluate its potential diagnostic application, we tested the antiserum's ability to bind HEV using immune electron microscope (IEM) and affinity-capture reverse transcription polymerase chain reaction (RT-PCR) amplification. Antiserum to ORF-2 aggregated HEV virions as seen by electron microscopy, providing direct evidence that ORF-2 encodes a structural protein. Antiserum also captured HEV for RT-PCR amplification. This antiserum bound HEV from diverse origins (Asia, Africa, Mexico) at virus concentrations found in patient fecal specimens and bile from inoculated non-human primates. The specificity of the affinity binding was demonstrated when pre-immune sera or sera collected from mice injected with control DNA vector (lacking the HEV ORF-2 gene) failed to bind HEV for RT-PCR amplification and IEM. Specific RT-PCR amplification was confirmed by restriction enzyme digestion of PCR products. The sensitivity of the binding was evaluated by RT-PCR amplification of serially diluted bile containing a genetically divergent HEV, Mexico'86. HEV was detected in a 10(-8) dilution of this bile. This is the first report that antibodies elicited by a DNA vaccine recognize native HEV. Our results indicate that ORF-2 encodes a structural protein and that antiserum to this protein enables simple, sensitive, and specific HEV detection by affinity-capture RT-PCR.

Animals↗
PubMed1999

The renin-angiotensin system and blood pressure: differences between blacks and whites.

Although blacks have lower plasma renin activity compared to whites, the corresponding differences in serum angiotensin converting enzyme (ACE) levels have not been well studied. Furthermore, few studies have examined the relationship of renin activity and ACE levels to blood pressure (BP) in blacks. We addressed these questions in a cross-sectional study conducted in 110 blacks and 183 whites who were not on antihypertensive medications. Three BP readings were obtained during a clinic visit. Plasma renin activity was assayed by radioimmunoassay and serum ACE levels were measured by spectrophotometry. Mean systolic and diastolic BP were 122.6 and 77.9 mm Hg in the blacks, and 123.4 and 77.9 mm Hg in the whites, respectively. Plasma renin activity was significantly lower in the blacks compared to the whites (0.92 v 1.26 ng/mL/h, respectively, P < .05), but ACE levels were similar in both groups (28.8 v 29.6 U/L, respectively). Renin activity was significantly and inversely associated with systolic and diastolic BP in both the blacks and the whites. ACE levels, however, were inversely associated with BP in the blacks but positively associated with BP in the whites (P = .02 for interaction on diastolic BP), even after adjustment for age, gender, body mass index (BMI), alcohol consumption, and heart rate. The corresponding interaction between ACE level and race on systolic BP was of borderline significance (P = .06). These results suggest that levels of ACE are similar in blacks and whites but their association with BP is possibly reflecting underlying ethnic differences in regulation of BP.

Adult↗
PubMed1999

Expression of transglutaminase K in normal cervix tissue and cervix carcinomas.

The localization and expression of transglutaminase K has been investigated immunohistochemically in normal cervix tissue (n = 15) and in cervix carcinomas (n = 23). The distribution of the transglutaminase K was compared with the staining patterns of cytokeratin 10, Ki-67, p53, and oestrogen and progesterone receptors in these tumours. Weak to strong membrane-bound immunoreactivity for transglutaminase K was detected in almost all cervix carcinomas analyzed. The immunostaining was heterogeneous, with visual differences between individual tumour cells. 66.7% of normal cervix tissues revealed no immunoreactivity for the transglutaminase K. In normal cervix tissue, the immunoreactivity was confined to upper cervix layers, predominantly to the superficial and intermediate cell layers. The intensity of both the immunostaining and the number of transglutaminase K-positive cells were upregulated in cervix carcinomas as compared to normal cervix tissue. When the coexpressions of transglutaminase K with markers of proliferation and differentiation were analyzed, no statistically significant correlation was found. Our findings indicate that (1) transglutaminase K is upregulated at the protein level in cervix carcinomas as compared to normal cervix tissue; (2) upregulation of the transglutaminase K in cervix carcinoma is not exclusively induced by alterations of epithelial differentiation or proliferation, but by different, unknown mechanisms; and (3) upregulation of transglutaminase K in cervix carcinomas may play an important role for the regulation of tumour invasive properties by modulating cell-cell interactions.

Biomarkers↗
PubMed1999

Promotion of photodynamic therapy-induced apoptosis by stress kinases.

Photodynamic therapy (PDT), a cancer treatment that employs a photosensitizer and visible light, induces apoptosis in murine LY-R leukemic lymphoblasts and in CHO cells, but the rate and extent of apoptosis are much greater in LY-R cells. Three MAPK family members, ERK1/ERK2, SAPK/JNK, and p38/HOG, are important intermediates in signal transduction pathways. To ascertain whether activation of one or more MAPKs could mediate PDT-induced apoptosis, Western blot analysis has been performed on the proteins of LY-R and CHO cells at various times following lethal (90 - 99% cell kill) doses of PDT photosensitized by the phthalocyanine Pc 4. The blots were probed with antibodies to each of the proteins as well as antibodies specific for the activated (phosphorylated) forms of each kinase. Of the three MAPK types, only the p46 and p54 SAPK/JNKs were found to be activated by PDT in LY-R cells, with a maximum approximately threefold increase in the content of the phosphorylated forms reached in 30 - 60 min. An even larger relative activation was observed in CHO cells. PDT did not affect ERK and p38/HOG activation in LY-R cells. In the case of CHO cells, however, ERK2 was slightly activated at 5 min post-PDT, then declined, and p38/HOG was strongly activated from 5 to 60 min post-PDT. A specific inhibitor (PD98059) of MEK1, the kinase that activates ERK, had little or no effect on PDT-induced apoptosis in either LY-R or CHO cells. In contrast, a specific inhibitor of p38/HOG (SB202190) blocked PDT-induced apoptosis in LY-R cells with a lesser effect in CHO cells. The results suggest that both the SAPK and p38/HOG cascades can be stimulated by PDT and that the latter participates in both rapid and slow PDT-induced apoptosis. Furthermore, the high level of constitutively active p38/HOG in LY-R cells may poise those cells for rapid activation of apoptosis following PDT.

Animals↗