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At least 235 records · Page 13Linked to original sources
PubMed1999

Gradients in cytoplasmic calcium concentration ([Ca2+]i) in migrating human umbilical vein endothelial cells (HUVECs) stimulated by shear-stress.

Using a parallel-plate flow-chamber and confocal laser scanning microscopy (CLSM), we studied the distribution and temporal changes in intracellular Ca2+ concentration ([Ca2+]i) in migrating HUVECs stimulated by shear-stress. In the presence or absence of ATP, shear-stress (10 dyne/cm2) caused morphological change and migration of individual HUVECs in the random direction. After 120 minute exposure to shear-stress, 70% of the cells migrated in the direction of flow, whereas, as many as 30% of the cells migrated to the upstream against flow. A nonspecific plasma membrane Ca2+ channel blocker, Ni2+, abolished such responses markedly, suggesting that Ca2+ influx may be essential for shear-stress dependent morphological change and migration of HUVECs. Analysis of [Ca2+]i distribution revealed the appearance of localized [Ca2+]i elevation inside lamellipodium formed in the direction of cell migration. The localized rise in [Ca2+]i might be closely related with morphological change to regulate the direction of cell migration induced by shear-stress.

Adenosine Triphosphate↗
PubMed2006

ICAM-1 expression in adipose tissue: effects of diet-induced obesity in mice.

Obesity has been linked to cardiovascular disease, hypertension, diabetes and the metabolic syndrome, with elevated markers of systemic inflammation. Intercellular adhesion molecule-1 (ICAM-1) is a transmembrane adhesion molecule involved in leukocyte migration to sites of inflammation. In human obesity, elevated expression of the soluble form of ICAM-1 (sICAM-1) is positively correlated with abdominal fat deposition. Increases in adiposity have also been correlated with macrophage infiltration into adipose tissue. Here we investigate adipose tissue production and transcriptional regulation of ICAM-1 in a mouse model of dietary obesity. After feeding mice a high-fat diet, ICAM-1 expression in serum and adipose tissue was analyzed by ELISA, Northern blotting, real-time quantitative PCR, and flow cytometry. After 6 mo on the high-fat diet, sICAM-1 levels significantly correlated with body weight and abdominal fat mass. ICAM-1 mRNA was expressed in adipose tissue of mice, with significantly higher levels in males than females. After only 3 wk, there were adipose tissue-specific increases in mRNAs for ICAM-1, IL-6, and monocyte chemoattractant protein-1 (MCP-1) in male mice. Analysis of the stromal-vascular fraction of male adipose tissue revealed CD11b-negative cells with increased surface ICAM-1 and CD34. We also found two populations of F4/80+, CD11b+, ICAM-1+ cells, one of which also expressed CD14 and CD11c and was increased in response to a high-fat diet. These results indicate that within 3 wk on a high-fat diet, male mice exhibited significant increases in pro-inflammatory factors and immune cell infiltration in adipose tissue that may represent links between obesity and its associated inflammatory complications.

Adipose Tissue↗
PubMed2004

MCP-1 induces migration of adult neural stem cells.

As a model for brain inflammation we previously studied transcriptional profiles of tumor necrosis factor-alpha (TNF)treated U373 astroglioma cells. In previous work we were able to demonstrate that the chemokine monocyte chemoattractant protein-1 (MCP-1, SCYA2, CCL2, MCAF) expression in U373 cells was inducible by TNF-alpha treatment. Demonstrably MCP-1 mRNA and protein expression in U373 cells was sustainable over time and at the highest level of all genes analyzed (Schwamborn et al., BMC Genomics 4, 46, 2003). In the hematopoietic system MCP-1 is a CC chemokine that attracts monocytes, memory T lymphocytes, and natural killer cells. In search of further functions in brain inflammation we tested the hypothesis that MCP-1 acts as a chemokine on neural stem cells. Here we report that MCP-1 activates the migration capacity of rat-derived neural stem cells. The migration of stem cells in a Boyden chamber analysis was elevated after stimulation with MCP-1. Time-lapse video microscopy visualized the migration of single stem cells from neurospheres in MCP-1-treated cultures, whereas untreated cultures depicted no migration at all, but showed signs of sprouting. Expression of the MCP-1 receptor CCR2 in neurosphere cultures was verified by RT-PCR and immunofluorescence microscopy. Supernatants from TNF-treated U373 cells also induced migration of neural stem cells.

Animals↗
PubMed1998

Seasonal changes in adrenal sensitivity alter corticosterone levels in Gambel's white-crowned sparrows (Zonotrichia leucophrys gambelii).

Recent work indicates that Gambel's white-crowned sparrows modulate corticosterone release seasonally in response to capture and restraint. Free-living white-crowned sparrows dramatically elevate both baseline and stress-induced corticosterone levels during the breeding season compared with either wintering or migrating birds. Although corticosteroid binding globulin capacity also rises during breeding, it does not fully compensate for elevated glucocorticoid levels. Consequently, we examined what hypothalamic-pituitary-adrenal axis changes could account for seasonal changes in glucocorticoid levels. During winter and fall migration, exogenous ACTH failed to elevate corticosterone levels beyond the response to capture and handling, suggesting that the adrenal's ability to release corticosterone limits circulating levels during these seasons. In contrast, not only were corticosterone levels higher during breeding, but adrenals further responded to an exogenous ACTH signal, indicating a dramatic enhancement of the adrenal's ability to secrete corticosterone. Furthermore, we inferred the pituitary's ACTH secretory ability by injecting exogenous corticotrophin-releasing factor (CRF), arginine vasotocin (AVT) and mesotocin and measured corticosterone release. Pituitaries in breeding birds appear to respond to exogenous CRF and AVT, suggesting hypothalamic control of corticosterone release during this season. Taken together, these results suggest that seasonal modulation of corticosterone release in this species is controlled primarily at the adrenal.

Adrenal Glands↗
PubMedDate not supplied

Retinal endothelial angiogenic activity: effects of hypoxia and glial (Müller) cells.

OBJECTIVE: To explore the impact of retinal glial (Müller) cells on survival and neovascularization-related activities of cultured retinal endothelial cells under normoxic and hypoxic conditions. METHODS: Bovine retinal endothelial cells (BRECs) were cultured under normoxia or hypoxia (0.5% O2) either alone, together with the human Müller cell line MIO-M1, or in normoxia- or hypoxia-conditioned media of MIO-M1 cells. Cell number, proliferation, apoptotic cell death, and migration of BRECs were determined. RESULTS: Exposure of BRECs to hypoxia for 24 h decreased the number of adherent cells and the proliferation rate, but increased apoptosis and cell migration. Increased apoptosis and decreased proliferation of the BRECs occurred also in the presence of conditioned media of MIO-M1 cells. Under normoxic conditions, co-culture with MIO-M1 cells resulted in increased proliferation, but decreased apoptosis and migration rates of BRECs. Under hypoxic conditions, the Müller cells released elevated amounts of VEGF but their presence decreased proliferation, apoptosis and the migration rates of BRECs. CONCLUSIONS: Hypoxia inhibits the proliferation of retinal endothelial cells. Müller cells release soluble mediators that enhance this hypoxia-mediated effect but, under certain conditions (i.e., in co-culture), may protect retinal endothelial cells from apoptosis, thus supporting their survival. Altogether the findings indicate that the key signal necessary to trigger retinal endothelial proliferation under hypoxia remains to be determined.

Animals↗
PubMed1996

Role of RuvA in branch migration reactions catalyzed by the RuvA and RuvB proteins of Escherichia coli.

The RuvA and RuvB proteins of Escherichia coli promote ATP-dependent branch migration of Holliday junctions during homologous genetic recombination and DNA repair. In this process, RuvA acts as a specificity factor that targets RuvB, a hexameric ring motor protein, to the junction. Because elevated concentrations of RuvB can promote branch migration in the absence of RuvA, it has been suggested that RuvA acts as a molecular matchmaker. In the studies presented here, we compared the requirements for RuvAB- and RuvB-mediated branch migration reactions and found that reactions catalyzed by RuvB alone were highly sensitive to inhibition by NaCl, temperature, ADP, and ATPgammaS. Our observations indicate that the two reactions occur by distinct mechanisms and support the notion that RuvAB-mediated branch migration is physiologically more relevant than that catalyzed by RuvB. We also show that ongoing RuvAB-mediated branch migration reactions were blocked by the addition of polyclonal antibodies raised against RuvA. The role of RuvA is therefore unlikely to be restricted to RuvB targeting; instead, it is required continually during branch migration. Competition with excess synthetic Holliday junctions, sufficient to sequester released RuvA, failed to cause an immediate block and leads us to suggest that RuvAB promote branch migration by a processive mechanism.

Adenosine Diphosphate↗
PubMed1999

Regulation of rat mesangial cell migration by platelet-derived growth factor, angiotensin II, and adrenomedullin.

This study sought to determine whether platelet-derived growth factor (PDGF) and angiotensin II (AngII) stimulate migration of cultured rat glomerular mesangial cells. After finding that this was so, the effects of adrenomedullin (ADM) and cAMP-elevating agents on basal and stimulated mesangial cell migration were examined. Two isoforms of PDGF, AB and BB, stimulated migration in a concentration-dependent manner between 1 and 50 ng/ml, while the AA isoform lacked significant effect. AngII modestly but significantly stimulated migration in a concentration-dependent manner between 10(-7) and 10(-6) mol/L. Rat ADM significantly inhibited the PDGF BB- and AngII-stimulated migration in a concentration-dependent manner between 10(-8) and 10(-7) mol/L. Inhibition by rat ADM was accompanied by an increase in cellular cAMP. cAMP agonists or inducers such as 8-bromo cAMP, forskolin, and prostaglandin I2 also significantly reduced the stimulated migration. H 89, a protein kinase A (PKA) inhibitor, attenuated the inhibitory effect of ADM, and a calcitonin gene-related peptide (CGRP) receptor antagonist, human CGRP (8-37), abolished the inhibitory effects of rat ADM. These results suggest that PDGF AB and BB as well as AngII stimulate rat mesangial cell migration and that ADM can inhibit PDGF BB- and AngII-stimulated migration, at least in part through cAMP-dependent mechanisms likely to involve specific ADM receptors with which CGRP interacts. The adenylate cyclase/cAMP/PKA system may be involved in the migration-inhibitory effect of ADM in these cells.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2005

Immunohistological characterization of macrophage migration inhibitory factor expression in Plasmodium falciparum-infected placentas.

Previously, we have shown that macrophage migration inhibitory factor (MIF) was highly elevated in the placental intervillous blood (IVB) of Plasmodium falciparum-infected women. Here, we compared the expression of MIF in placental tissues obtained from P. falciparum-infected and -uninfected women. Immunoperoxidase staining showed a consistent pattern of MIF expression in syncytiotrophoblasts, extravillous trophoblasts, IVB mononuclear cells, and amniotic epithelial cells, irrespective of their malaria infection status. Cytotrophoblast, villous stroma, and Hofbauer cells showed focal staining. Only amniotic epithelial and IVB mononuclear cells from P. falciparum-infected placentas exhibited significantly higher level of MIF expression than uninfected placentas. Stimulation of syncytilized human trophoblast BeWo cells with P. falciparum-infected erythrocytes that were selected to bind these cells resulted in significant increases in MIF secretion, whereas control erythrocytes, lipopolysaccharides, and synthetic beta-hematin had minimal effect. These findings suggest that placental malaria modulates MIF expression in different placental compartments.

Animals↗
PubMed2005

Promoter region polymorphism of macrophage migration inhibitory factor is strong risk factor for young onset of extensive alopecia areata.

We have demonstrated that serum macrophage migration inhibitory factor (MIF) was significantly elevated in patients with extensive alopecia areata (AA). Recently, functional polymorphisms have been identified in the MIF promoter region. To address the functional and prognostic relevance of the -173G/C and -794[CATT]5-8 repeat polymorphisms in MIF genes in patients with extensive AA, 113 patients with extensive AA and 194 healthy controls were genotyped. We found that MIF-173*C was a risk factor for early onset (<20 years) of extensive AA (odds ratio for GC heterozygotes with -173G/C was 4.88 (95% CI, 2.04-11.8), P=0.00038; odds ratio for CC homozygotes with -173G/C was 10.42 (95% CI, 2.56-43.5), P=0.0011). We found no statistically significant differences in the genotype frequencies of the -794[CATT]5-8 repeat polymorphism and extensive AA. These results suggest that polymorphisms within the MIF-173*C allele confer an increased risk of susceptibility to the extensive forms of AA, especially with an early onset of disease. MIF is therefore suggested to be closely implicated in the pathogenesis of the more extensive forms of AA.

Adolescent↗
PubMed2006

Interleukin-8: novel roles in human airway smooth muscle cell contraction and migration.

In patients with cystic fibrosis (CF) and asthma, elevated levels of interleukin-8 (IL-8) are found in the airways. IL-8 is a CXC chemokine that is a chemoattractant for neutrophils through CXCR1 and CXCR2 G protein-coupled receptors. We hypothesized that IL-8 acts directly on airway smooth muscle cells (ASMC) in a way that may contribute to the enhanced airway responsiveness and airway remodeling observed in CF and asthma. The aim of this study was to determine whether human ASMC (HASMC) express functional IL-8 receptors (CXCR1 and CXCR2) linked to cell contraction and migration. Experiments were conducted on cells harvested from human lung specimens. Real-time PCR and fluorescence-activated cell sorting analysis showed that HASMC expressed mRNA and protein for both CXCR1 and CXCR2. Intracellular Ca(2+) concentration ([Ca(2+)](i)) increased from 115 to 170 nM in response to IL-8 (100 nM) and decreased after inhibition of phospholipase C (PLC) with U-73122. On blocking the receptors with specific neutralizing antibodies, changes in [Ca(2+)](i) were abrogated. IL-8 also contracted the HASMC, decreasing the length of cells by 15%, and induced a 2.5-fold increase in migration. These results indicate that HASMC constitutively express functional CXCR1 and CXCR2 that mediate IL-8-triggered Ca(2+) release, contraction, and migration. These data suggest a potential role for IL-8 in causing abnormal airway structure and function in asthma and CF.

Antibodies↗
PubMed1998

Cytokines stimulate matrix metalloproteinase production by human pulp cells during long-term culture.

Interleukin-1 and tumor necrosis factor-alpha are inflammatory cytokines that are known to be potent stimulators of mineralized tissue resorption. One of the mechanisms by which these cytokines induce this loss is through the stimulation of matrix metalloproteinase (MMP) production and secretion by the host cells present at the inflammatory site. We have previously shown that these cytokines have little effect on MMP production by human pulp cells in short-term culture (24 to 48 h). In this study, we examined the production of MMPs by human pulp cells in the presence and absence of interleukin-1 and tumor necrosis factor-alpha in long-term cultures (2 to 16 days) using substrate gel zymography. The major band present in all samples examined migrated at 68 kDa, corresponding to the migration pattern of MMP-2, whereas a minor band migrated at 90 kDa, corresponding to the migration pattern of MMP-9. In the presence of cytokines, elevated levels of MMP-2 and MMP-9 were apparent at days 9 through 16. In addition, a band migrating at 110 kDa was present. This study demonstrates that cytokines stimulate the production of elevated levels of MMPs by human pulp cells in long-term cultures and that these MMPs may play a role in pulpal inflammation.

Cells, Cultured↗
PubMed1993

Chemotaxis of newt eosinophils: calcium regulation of chemotactic response.

Local chemical events underlying chemotaxis were characterized in a new model cell, the newt eosinophil. These cells exhibit a chemotactic response to a trypsin-sensitive component of newt serum. Ca2+ plays a role in this process, since treatments expected to diminish Ca2+ availability from the medium [ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid, Co2+, and verapamil], to break down transmembrane Ca2+ gradients (ionomycin), or to interfere with the function of intracellular Ca2+ stores (caffeine and neomycin) inhibited cell polarization and movement. Using imaging techniques we found that cytosolic Ca2+ concentration ([Ca2+]i) increased in response to newt serum. Migrating newt eosinophils exhibited a dynamic heterogeneous distribution of [Ca2+]i. [Ca2+]i was elevated in cells undergoing a change of direction relative to cells migrating persistently in one direction. Migrating cells contained gradients of [Ca2+]i along their long axis, with the front of the cell having consistently lower [Ca2+]i than the rear. When cells were loaded with the cell-permeant form of fura 2, fura 2 acetoxymethyl ester, a caffeine-sensitive membrane-delimited region of elevated [Ca2+]i was seen associated with the microtubule organizing center. A model is proposed relating the distribution of [Ca2+]i and the location of the external stimulus to the generation and interaction of substances within the cell that both simulate and inhibit increases in [Ca2+]i.

Amino Acid Sequence↗
PubMed2004

Rhodium-catalyzed intramolecular hydroacylation of 5- and 6-alkynals: convenient synthesis of alpha-alkylidenecycloalkanones and cycloalkenones.

A novel intramolecular hydroacylation of 5- and 6-alkynals leading to alpha-alkylidenecycloalkanones was accomplished by using cationic a rhodium(I)/BINAP complex. For all cyclizations described, a single (E)-olefin isomer was obtained. At elevated temperature, hydroacylation and double bond migration of 5- and 6-alkynals proceeded in a one-pot reaction to give cycloalkenones. An intramolecular hydroacylation of a 7-alkynal was unsuccessful. This method represents an attractive new route to highly functionalized alpha-alkylidenecycloalkanones and cycloalkenones.

Acylation↗
PubMed2004

Responses and signaling pathways in human optic nerve head astrocytes exposed to hydrostatic pressure in vitro.

In this study, we examined the effects of mechanical stress induced by elevated hydrostatic pressure (HP) on the migration of human optic nerve head (ONH) astrocytes, using an in vitro model that follows repopulation of a cell-free area (CFA) created on a monolayer of cultured astrocytes. alpha-Tubulin staining detected phenotypic changes in astrocytes exposed to HP. The influence of proliferation in closure of the CFA was determined by incorporation of BrdU under 1.5-cm H2O, control pressure (CP), and 10-cm H2O HP with or without 5-fluorouracil. Under control and experimental conditions, closure of the CFA occurred mostly by migration and less by proliferation. Exposure to 10-cm H2O HP induced faster closure of the CFA at 1, 3, and 5 days. The signaling pathways involved in responses to HP were determined using genistein, tyrphostin A25, AG1478, and AG1295, inhibitors of receptor tyrosine kinases; wortmannin and LY294002, inhibitors of phosphatidyl inositol 3-kinase (PI-3K); and SC58236, an inhibitor of inducible cyclooxygenase-2 (COX2). Genistein and tyrphostin A25 blocked HP-induced migration at 1, 3, and 5 days, but did not affect closure of the CFA under CP. AG1478 and AG1295 blocked HP-induced migration and partially inhibit closure of the CFA under CP. LY294002 blocked HP-induced migration. SC58236 markedly inhibited closure of the CFA under CP by inhibiting COX2 activity. Exposure to HP, a physical stress, induced faster closure of the CFA via activation of members of the epidermal growth factor receptor (EGFR) family and PI-3K pathways. Under CP, closure of the CFA in response to denudation, a form of injury, is due to activation of COX2 in ONH astrocytes.

Adolescent↗
PubMed1998

Endocrine profiles of female striped bass (Morone saxatilis) in captivity, during postvitellogenesis and induction of final oocyte maturation via controlled-release GnRHa-delivery systems.

Plasma levels of reproductive and thyroid hormones were measured in captive striped bass females during postvitellogenesis and the spawning period (March-June). Circulating gonadotropin II (GtH II), 17,20beta-dihydroxy-4-pregnen-3-one (17,20beta-P), and 17,20beta, 21-trihydroxy-4-pregnen-3-one (17,20beta,21-P) remained low and unchanged in nonmaturing females, while 17beta-estradiol (E2) and testosterone (T) declined throughout postvitellogenesis. Plasma thyroxine (T4) declined significantly in mid-April, while triiodothyronine (T3) increased in mid-May. The only female that ovulated spontaneously had markedly different E2, T, and T3 profiles during postvitellogenesis, and had a surge in plasma GtH II during final oocyte maturation (FOM). The lack of a GtH II surge is presumably responsible for the absence of FOM, but earlier, and as of yet unknown, endocrine disruptions during postvitellogenesis may determine the female's ability to undergo FOM. Treatment of females with a gonadotropin-releasing hormone agonist (GnRHa)-delivery system induced FOM and ovulation within 3 and 10 days, respectively, and resulted in the production of fertile eggs. Plasma GtH II increased continually after GnRHa implantation, even in the presence of declining GnRHa plasma levels. Plasma E2 increased first and peaked prior to FOM, whereas T peaked at the peripheral germinal vesicle (GV) stage. Plasma 17,20beta-P and 17,20beta,21-P increased dramatically at the GV breakdown (GVBD) stage. Plasma T4 was unaffected by the GnRHa treatment, whereas T3 decreased after GnRHa implantation and remained low throughout FOM. Based on the observed hormonal profiles, FOM can be separated into an early phase (lipid-droplet coalescence, GV migration) associated with E2 and T elevations, and a late phase (yolk-globule coalescence, GVBD) associated with 17,20beta-P and 17,20beta,21-P elevation.

Animals↗
PubMed1985

Taenia pisiformis: protective immunization of rabbits with solubilized oncospheral antigens.

Antigens were derived from hatched and activated oncospheres of Taenia pisiformis which had been separated from embryophoric debris by centrifugation on Percoll. Crude oncospheral antigen was prepared by freeze-thawing and sonication of oncospheres at 4 C, and a supernatant of crude antigen was collected following centrifugation at 100,000g. Other antigens tested were the supernatants collected after 100,000g centrifugation of crude antigen solubilized in Triton X-100, butanol, lithium diiodosalicylic acid, KCl, sodium dodecyl sulfate, or sodium deoxycholate. When groups of rabbits were immunized with the various antigens and challenged with T. pisiformis eggs, both sodium deoxycholate- and Triton X-100-solubilized antigens stimulated a level of protection similar to the crude antigen. All other antigens failed to stimulate significant protective immunity. When sodium deoxycholate-solubilized antigen was fractionated using high-performance liquid chromatography, the major host-protective components were in the fractions with molecular weight greater than 140,000. Levels of the enzyme, glutamate dehydrogenase (EC 1.4.1.2), in the serum of rabbits challenged with T. pisiformis eggs closely reflected the degree of liver damage caused by migrating larvae, and were not markedly elevated in those rabbits effectively immunized using the crude or sodium deoxycholate-solubilized antigens.

Animals↗
PubMed1991

Developmental differences in the responsiveness of gill Na+,K(+)-ATPase to cortisol in salmonids.

The ability of cortisol to increase gill Na+,K(+)-ATPase activity was examined in several salmonid species during development. Coho salmon (Oncorhynchus kisutch) parr were unresponsive to cortisol in vitro (10 micrograms/ml for 2 days) in November. Responsiveness was significant from January to March, peaking in January just prior to seasonal increases in gill Na+,K(+)-ATPase activity. Gill tissue became unresponsive to in vitro cortisol in April when in vivo gill Na+,K(+)-ATPase activity peaked. The ability of cortisol to stimulate gill, Na+,K(+)-ATPase activity in postemergent fry (2-3 months after hatching) was examined in chum (O. keta), chinook (O. tschawytscha), coho, and Atlantic salmon (Salmo salar). Initial levels of gill Na+,K(+)-ATPase activity were elevated in chum salmon, which normally migrate as fry. Cortisol (10 micrograms/ml for 4 days in vitro) increased gill Na+,K(+)-ATPase activity in chum salmon fry (48% above initial levels), had a limited but significant effect in chinook salmon fry, and had no effect in coho and Atlantic salmon fry. In an in vivo experiment, Atlantic salmon previously exposed to simulated natural photoperiod (SNP) and continuous light (L24) received four cortisol injections of 2 micrograms.g-1 every third day. SNP fish responded with increased gill Na+,K(+)-ATPase activity (+66%), whereas L24 fish were not affected. Atlantic salmon presmolts with initially low levels of gill Na+,K(+)-ATPase activity responded to cortisol in vitro, whereas smolts with initially high levels of gill Na+,K(+)-ATPase activity were unresponsive.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Year-to-year differences in plasma levels of steroid hormones in pre-spawning chum salmon.

Changes in plasma levels of steroid hormones in pre-spawning chum salmon (Oncorhynchus keta) were examined for 6 years in association with sexual maturation. Fish were sampled along their homing pathway from the coastal sea to the spawning ground from 1995 to 2000. Plasma levels of testosterone (T), 11-ketotestosterone (11KT), estradiol-17beta (E2), 17alpha,20beta-dihydroxy-4-pregnen-3-one (DHP), and cortisol were determined by enzyme immunoassays. Sexual maturity was comprehensively estimated by gonadosomatic indices, histology of gonads, nuptial color, spermiation or ovulation ratio. Since the plasma levels of steroid hormones and sexual maturation differed from year to year, they were compared with year-to-year variation of sea surface temperature (SST) of coastal sea to study influence of oceanographic environment on these physiological data. The SST of the migratory route varied among the years, so that we classified the 6 years into cool, intermediate, and warm years. Concerning maturity, the males that returned to the natal hatchery in the warm years were sexually more advanced than those in the cool years. Furthermore, histological data suggested that final oocyte maturation occurred before arrival at the hatchery in one of the warm years, i.e., 1999, while it occurred at the hatchery in one of the intermediate years, i.e., 2000. In the males, T and 11KT levels increased significantly on midway of the homing route in the warm years, whereas they did not show any noticeable changes in the cool years. Furthermore, the levels of T and 11KT on midway of the homing route in the warm years, i.e., 1998 and 1999, were significantly higher than those in one of the cool years, i.e., 1995, in both sexes. In the females, the levels of E2 decreased during upstream migration. Conversely, those of DHP considerably elevated at spawning ground in all years examined. The levels of cortisol were different from year to year regardless of the SST. The present results showed that there were year-to-year differences in plasma levels of steroid hormones and maturity, and some of them may be influenced by the year-to-year variation of SST.

Animals↗