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Biomedical subjects

H Ichikawa

Publications and source records attributed to H Ichikawa.

At least 181 records · Page 10Linked to original sources

A comparison of the University of Wisconsin solution and the modified Kawakami solution for initial flush and coronary perfusion in long-term canine heart preservation.

BACKGROUND: We compared two different solutions, the University of Wisconsin (UW) solution (intracellular-like) and the modified Kawakami (mK) solution (extracellular-like), for initial flush of coronary vascular beds before simple storage and following coronary perfusion. METHODS: After a right thoracotomy in the 4th intercostal space, the donor heart was isolated by ligating the azygos vein and venae cavae, and cross-clamping the aorta. Cardiac arrest was then obtained with a cold GIK solution. Following initial flush of coronary vascular beds, the donor heart was resected, stored utilizing a combination of simple immersion and coronary perfusion, and then transplanted. A total of 48 mongrel dogs was divided into three groups each using different solutions for the initial flush of coronary vascular beds and for coronary perfusion. In group I (n=10) the UW solution was used for both initial flush and coronary perfusion. In group II (n=7) the mK solution was used for both initial flush and coronary perfusion, and in group III (n=7) the UW solution was used for initial flush and the mK solution for coronary perfusion. Intracellular high-energy phosphate was surveyed by 31P-nuclear magnetic resonance spectroscopy. RESULTS: After 12-hour simple immersion and 1-hour coronary perfusion, phosphocreatine and adenosine triphosphate were significantly (p<0.05) higher in group III than in groups I and II. The high-energy phosphate levels of the graft tissue were better in groups I and III than in group II. Orthotopic transplantation was then performed using 10 preserved grafts in group I and seven preserved grafts of group III. After transplantation, left ventricular (LV) pressure of group I animals recovered to 82.3% and group III recovered to 95.8% of the control values. LV dp/dt of group I and III animals recovered to 76.5% and 96.7% of the control values, respectively. CONCLUSIONS: The UW solution, which is acceptable for both initial flush and simple storage, is not suitable for continuous coronary perfusion even for a short period due to its high viscosity. A combination of the UW solution both for initial flush and the following cold simple immersion and the mK solution for continuous coronary perfusion is appropriate for long-term preservation of the canine heart.

Adenosine↗

Coexpression of calretinin and parvalbumin in Ruffini-like endings in the rat incisor periodontal ligament.

The coexpression of calretinin- (CR) and parvalbumin-immunoreactivities (irs) was examined in oro-facial tissues of the rat. Nerve fibers coexpressing these calcium-binding proteins (CaBPs) were observed in the lingual periodontal ligament of incisors but not other tissues. In the part of periodontal ligament adjacent to the alveolar bone, such nerve fibers left nerve bundles and formed bush-like endings, i.e., they ramified repeatedly and terminated with one to four twigs. An immunoelectron microscopic method indicated that these endings were identical to Ruffini-like endings, 4% of trigeminal neurons retrogradely labeled from the inferior alveolar nerve coexpressed CR- and parvalbumin-irs. The present observations suggest that the coexpression of these CaBPs may be a specific marker for low-threshold mechanoreceptors in the trigeminal ganglion.

Animals↗

Cytoskeletal rearrangements and transcriptional activation of c-fos serum response element by Rho-kinase.

The small GTPase Rho is implicated in cytoskeletal rearrangements including stress fiber and focal adhesion formation and in the transcriptional activation of c-fos serum response element. In vitro, Rho-kinase, which is activated by Rho, phosphorylates not only myosin light chain (MLC) (thereby activating myosin ATPase) but also myosin phosphatase, thus inactivating myosin phosphatase. Rho-kinase is involved in the formation of stress fibers and focal adhesions in fibroblasts. Here we show that the expression of constitutively active Rho-kinase increased the level of MLC phosphorylation. The activity of Rho-kinase was necessary for maintaining the vinculin-containing focal adhesions, whereas organized actin stress fibers were not necessary for this. The microinjection of constitutively active Rho-kinase into fibroblasts induced the formation of focal adhesions to some extent under the conditions where organized actin stress fibers were disrupted. The expression of constitutively active Rho-kinase also stimulated the transcriptional activity of c-fos serum response element. These results suggest that Rho-kinase has distinct roles in divergent pathways downstream of Rho, which include MLC phosphorylation leading to stress fiber formation, focal adhesion formation, and gene expression.

3T3 Cells↗

Coexistence of calcium-binding proteins in vagal and glossopharyngeal sensory neurons of the rat.

The presence and coexistence of the calcium-binding proteins (CaBPs), calbindin D-28k, parvalbumin and S100 protein, were immunohistochemically examined in the glossopharyngeal and vagal sensory ganglia, the carotid body and taste buds. The CaBPs were found in each ganglion with the nodose ganglion containing the largest number of CaBP-immunoreactive (ir) cells (calbindin D-28k > or = S100 >> parvalbumin). The coexistence of CaBPs was found in neurons of the nodose, petrosal, and jugular ganglia. Calbindin D-28k-ir neurons in the nodose and petrosal ganglia frequently colocalized S100-ir whereas calbindin D-28k-ir neurons in the jugular ganglion less frequently contained S100-ir. Only small percentages of calbindin D-28k-ir neurons in each ganglion colocalized parvalbumin. Similarly, S100-ir neurons in the nodose and petrosal ganglia frequently colocalized calbindin D-28k-ir whereas S100-ir neurons in the jugular ganglion less frequently contained calbindin D-28k-ir. Moderate to small percentages of S100-ir neurons in each ganglion colocalized parvalbumin. Parvalbumin-ir neurons nearly always colocalized S100-ir in the nodose, petrosal and jugular ganglia. Moderate to small percentages of parvalbumin-ir neurons in each ganglion colocalized calbindin D-28k. Whereas calbindin D-28k- and S100-ir were colocalized in nerve fibers and cells within taste buds of circumvallate papilla of the tongue, the coexistence of these CaBPs could not be determined in the carotid body. These findings suggest a co-operative role for CaBPs in the functions of subpopulations of nodose and petrosal ganglia neurons.

Animals↗

Consistent detection of TLS/FUS-ERG chimeric transcripts in acute myeloid leukemia with t(16;21)(p11;q22) and identification of a novel transcript.

16;21 translocation is a recurrent primary abnormality in acute myeloid leukemia (AML). The genes involved in this translocation are ERG on chromosome 21 and TLS/FUS on chromosome 16. The rearrangement of the two chromosomes forms the TLS/FUS-ERG fusion gene and produces a consistent chimeric transcript on the der (21) chromosome. In this study, we analyzed the clinical characteristics of 19 patients with t(16;21)-AML, including 2 patients who evolved from myelodysplastic syndrome, and detected the chimeric transcripts of the TLS/FUS-ERG fusion gene in the patients during various clinical stages by the reverse transcriptase-polymerase chain reaction (RT-PCR) technique. We found that the patients with t(16;21) are characterized by a relatively younger age (median age, 22 years old), involvement of various subtypes of French-American-British classification and a poor prognosis: 18 of the 19 patients died of the disease (median survival was 16 months). Four types of TLS/FUS-ERG chimeric transcripts including a novel type were noted in the RT-PCR analysis. The novel transcript contained an additional 138 nucleotides consisting of TLS/FUS exon 8 and ERG exons 7 and 8 and had an in-frame fusion. These chimeric transcripts were consistently detectable in the samples obtained not only at diagnosis and relapse but also in short and long complete remission, suggesting that t(16;21)-AML is resistant to conventional chemotherapy. Thus, we recommend that t(16;21) should be monitored by RT-PCR even in clinical remission and the patients should be treated by other more powerful modality like stem-cell transplantation in the first remission.

Acute Disease↗

A silent mutation in the ftsH gene of Escherichia coli that affects FtsH protein production and colicin tolerance.

Among Escherichia coli tolZ mutants tolerant to colicins E2, E3, and D, one, KHI10, had a high frequency of lambda lysogenization, like the tolZ21 mutant, but unlike tolZ21 KHI10 grew on nonfermentable carbon sources. The tolZ10 gene of KHI10 was cloned and sequenced, and found to have a silent mutation in the ftsH gene, causing an alteration of a minor codon, CUA, for Leu-5 to a suboptimal codon, CUC. In spite of the change in a minor codon, the amount of the FtsH protein present in mutant cells was much less than that in the parental strain. In vivo transcription of the tolZ10 gene was not decreased relative to the wild-type ftsH gene. Analysis of other silent mutations altering the Leu-5 codon (CUA) to CUG or CUU (optimal and suboptimal codons, respectively) revealed that the decrease in concentration of FtsH was seen only with the CUC (tolZ10) codon. Prediction of the mRNA secondary structure suggested that the change from A to C extends the base pairing region longer by one base pair at the root of the stem structure, thus sequestering the Shine-Dalgarno sequence and decreasing the rate of the translational initiation of FtsH.

ATP-Dependent Proteases↗

Cloning of a mRNA preferentially expressed in chondrocytes by differential display-PCR from a human chondrocytic cell line that is identical with connective tissue growth factor (CTGF) mRNA.

Chondrocyte- or chondrosarcoma cell line (HCS)-specific DNA fragments were obtained using differential display-PCR. Nucleotide sequences of 32 species derived from HCS cells were determined. One of the sequence tags (tag no. 24) corresponded to the nucleotide sequence of connective tissue growth factor (CTGF). Northern blot analysis showed that CTGF was highly expressed in HCS cells and rabbit growth cartilage cells in culture but was not expressed in osteoblastic cells in culture. In situ hybridization revealed that CTGF was expressed only in the hypertrophic chondrocytes of costal cartilage and the vertebral column in embryonic mice. The expression of CTGF in HCS cells was up-regulated by the addition of TGF-beta or BMP-2. These findings suggest that CTGF participates in endochondral ossification.

Animals↗

In vivo gene transfection with heat shock protein 70 enhances myocardial tolerance to ischemia-reperfusion injury in rat.

Heat shock protein 70 (HSP70) has been reported to be involved in the myocardial self-preservation system. To obtain the evidence that HSP70 plays a direct role in the protection from myocardial ischemia-reperfusion injury, rat hearts were transfected with human HSP70 gene by intracoronary infusion of hemagglutinating virus of Japan (HVJ)-liposome containing human HSP70 gene. The control hearts were infused with HVJ-liposome without the HSP70 gene. The hearts from whole-body heat-stressed or nontreated rats were also examined. Western blot and immunohistochemical analysis showed that apparent overexpression of HSP70 occurred in the gene transfected hearts and that gene transfection might be more effective for HSP70 induction than heat stress. In Langendorff perfusion, better functional recovery as well as less creatine phosphokinase leakage after ischemia were obtained in the gene transfected hearts with HSP70 than in the control or nontreated hearts. Furthermore, the gene transfected hearts showed better functional recovery than the heat-stressed hearts. These results indicated that overexpressed HSP70 plays a protective role in myocardial injury, suggesting the possibility that gene transfection with HSP70 may become a novel method for myocardial protection through enforcing the self-preservation systems.

Animals↗

Central projection of calcitonin gene-related peptide (CGRP)- and substance P (SP)-immunoreactive trigeminal primary neurons in the rat.

Substance P (SP) is implicated in transmission of primary afferent nociceptive signals. In primary neurons, SP is colocalized with calcitonin gene-related peptide (CGRP), which is another neuropeptide marker for small to medium primary neurons. CGRP coreleased with SP augments the postsynaptic effect of SP and thereby modulates the nociceptive transmission. This study demonstrates the distribution of CGRP-like immunoreactivity (-ir) and SP-ir in the lower brainstem of normal rats and after trigeminal rhizotomy or tractotomy at the level of subnucleus interpolaris (Vi). By comparing the results obtained from normal and deafferented rats, we analyzed the central projection of trigeminal primary nociceptors. The CGRP-immunoreactive (-ir) trigeminal primaries projected to the entire rostrocaudal extent of the spinal trigeminal nucleus, the principal nucleus (PrV), the paratrigeminal nucleus (paraV), and the lateral subnucleus of solitary tract nucleus (STN) on the ipsilateral side. The trigeminal primaries projecting to the spinal trigeminal nucleus, paraV and STN also contained SP-ir. The ipsilateral trigeminal primaries were the exclusive source of CGRP-ir terminals in the PrV, the Vi and the dorsomedial nucleus within the subnucleus oralis (Vo). The medullary dorsal horn (MDH) and the lateral edge of Vo received convergent CGRP-ir projection from the ipsilateral trigeminal primaries and other neurons. The glossopharyngeal and vagal primaries are candidates for the source of CGRP-ir projection to the Vo and the MDH, while the dorsal root axons supply the MDH with CGRP-ir terminals. In addition, contralateral primary neurons crossing the midline appear to contain CGRP and to terminate in the MDH.

Animals↗

S100 protein-immunoreactive primary sensory neurons in the trigeminal and dorsal root ganglia of the rat.

The cell body size (cross-sectional area) of S100-immunoreactive (-ir) primary neurons was measured in the trigeminal (TG) and lumbar dorsal root ganglia (DRG). About a half of neurons exhibited S100-immunoreactivity (-ir) in the DRG (44.0%) and TG (59.0%). DRG neurons with cell bodies > 1200 microm2 mostly exhibited S100-ir (96.5%), whereas S100-ir DRG neurons < 600 microm2 were rare (8.0%). 36.6% of DRG neurons in the cell size range 600-1200 microm2 showed the ir. TG neurons > 800 microm2 mostly exhibited S100-ir (93.1%), whereas those < 400 microm2 were devoid of it (positive cells 10.5%). 58.3% of TG cells in the range 400-800 microm2 contained S100-ir. Double-immunofluorescence method revealed the co-expression of S100 and other calcium-binding proteins. Parvalbumin-ir neurons mostly exhibited S100-ir in the DRG (97.4%) and TG (97.0%). The co-expression of S100 and calbindin D-28k was very rare in the DRG, because the DRG contained few calbindin D-28k-ir neurons. Unlike in the DRG, numerous neurons co-expressed S100- and calbindin D-28k-ir in the TG. Most calbindin D-28k-ir TG neurons were also immunoreactive for S100 (90.7%). Sub-populations of calretinin (CR)-ir neurons co-expressed S100-ir in both the DRG (68%) and TG (50.0%). Virtually all CR-ir neurons > 1400 microm2 co-expressed S100-ir in the DRG (100%) and TG (95.9%). CR-ir neurons < 800 microm2 were rarely exhibited S100-ir (DRG 18.0%, TG 21.9%). 71.3 and 60.5% of CR-ir neurons in the range 800-1400 microm2 co-expressed S100-ir in the DRG and TG, respectively. The present study indicates that S100 is closely correlated to the primary neuronal cell size in the DRG and TG.

Animals↗

Parvalbumin- and calbindin D-28k-immunoreactive innervation of orofacial tissues in the rat.

Parvalbumin- and calbindin D-28k-immunoreactive (-ir) innervation was examined in orofacial tissues of the rat. Labial and facial skins were devoid of the calcium-binding protein (CaBP)-ir nerve endings, while the infraorbital and mental nerves contained numerous parvalbumin-ir axons. Labial and gingival mucosae were also devoid of the CaBP-ir nerve endings. The buccal mucosa and incisive papilla contained both encapsulated and unencapsulated endings, while the hard palate mucosa excluding the incisive papilla contained only unencapsulated endings. Encapsulated endings were found just beneath the epithelium or attached to the cartilaginous core of the incisive papilla. Unencapsulated endings in the lamina propria were subdivided into two types: simple (unramified) and complex (ramified). Neurites of simple endings were straight, curved, or coiled, while those of complex endings exhibited a bush-like appearance due to the ramification. In addition, palatal rugae contained intraepithelial endings. The unencapsulated complex endings in palatal rugae coexpressed parvalbumin- and calbindin D-28k-irs, whereas other endings were immunoreactive for parvalbumin alone. The pterygopalatine ganglion contained calbindin D-28k-ir pericellular fibers but not the ir cell bodies. A subpopulation of trigeminal ganglion neurons coexpressed both CaBPs. CaBP-ir encapsulated and unencapsulated endings in the oral mucosa probably include low-threshold mechanoreceptors, while parvalbumin-ir intraepithelial endings in the palatal mucosa may be involved in nociception.

Animals↗

The contribution of Na+/H+ exchange to ischemia-reperfusion injury after hypothermic cardioplegic arrest.

BACKGROUND: Na+/H+ exchange has been reported to be one of the key mechanisms in myocardial ischemia-reperfusion injury. However, the effect of temperature on Na+/H+ exchange is not fully understood. METHODS: Sodium-propionate-induced cell swelling, an indicator of the function of the Na+/H+ exchanger, was measured in rat thymic lymphocytes. A Langendorff perfused rat heart model was also employed to investigate the effect of the pharmacologic inhibition of Na+/H+ exchange on the recovery of cardiac function after hypothermic ischemia. This was done using FR168888, an inhibitor of Na+/H+ exchange. RESULTS: In the in vitro study, rat lymphocytes were observed to swell at 17 degrees, 22 degrees, and 27 degrees C, indicating that the Na+/H+ exchanger remains functional even under hypothermic conditions. FR168888 was found to significantly inhibit Na+/H+ exchange-induced cell swelling, even at 17 degrees C. In the in vivo study, pretreatment with FR168888 was found to prevent the deterioration of ventricular function, even after 5 hours of hypothermic cardioplegic arrest. This was associated with a decrease in the reperfusion-induced elevation in resting tension. CONCLUSIONS: These results suggest that Na+/H+ exchange in the heart still occurs, even under hypothermic conditions, and contributes to reperfusion injury, even after hypothermic cardioplegic arrest.

Animals↗

Effect of cardiopulmonary bypass under tepid temperature on inflammatory reactions.

BACKGROUND: Cardiopulmonary bypass (CPB) causes inflammatory reactions and abnormal responses of vascular resistance. Theoretically, the difference in the blood temperature during CPB may influence the degree of CPB-induced inflammatory reactions. METHODS: To elucidate the effect of the perfusate temperature during CPB, serum levels of inflammatory cytokines, neutrophil elastase, complements, and vasoactive substances were measured in 18 patients undergoing elective coronary artery bypass grafting under tepid temperature (34 degrees C) and moderate hypothermia (28 degrees C). Respiratory index and systemic vascular resistance index during and after CPB and intubation time after postoperative course were also analyzed. RESULTS: The patterns of the change in interleukin-8 and neutrophil elastase were significantly different between the two groups. The tepid group showed an earlier decrease in interleukin-8 and neutrophil elastase levels as compared with the hypothermic group. The prostaglandin E2 level just after CPB was significantly higher in the tepid group than in the hypothermic group. Systemic vascular resistance index and respiratory index and intubation time were significantly lower in the tepid group than in the hypothermic group. CONCLUSIONS: These results demonstrated that tepid CPB affected the inflammatory cytokine release and neutrophil activation compared with hypothermic CPB, resulting in the attenuation of respiratory dysfunction. This may suggest a beneficial effect of tepid temperature in CPB with possible attenuation of the postperfusion syndrome.

Bradykinin↗

Exaggerated C-fiber activation prevents peripheral nerve injury-induced hyperinducibility of c-Fos in partially deafferented spinal dorsal horn.

Dorsal horn neurons chronically deafferented by peripheral nerve injuries acquire hypersensitivity to noxious input from outside the original receptive field. This study examines the effect of electrical nerve stimulation at the time of injury on such injury-induced hypersensitivity. The medial 3/8 of the dorsal horn laminae I/II around the junction of 4th and 5th lumbar segments (the tibial territory) was deafferented by transection of the ipsilateral tibial nerve in rats. At 2 days or 3 weeks postinjury, the hindpaw was injected with formalin to induce c-fos. At 2 days, neurons with induced c-Fos protein-like immunoreactivity (fos-neurons) were largely confined in the lateral 5/8 of laminae I/II (the peroneal and hip, thus P and H territory). At 3 weeks, fos-neurons significantly increased in the deafferented tibial territory. A similar increase was also noted in the P and H territory. Thus the dorsal horn neurons exhibited c-fos hyperinducibility, an indication of hypersensitivity. Electrical stimulation with a train of 150 shocks (10 V, 2 ms) of the proximal nerve stump immediately after transection prevented the c-fos hyperinducibility. The effect was greater with the stimulation frequency of 0.5 Hz than 0.1 Hz or 10 Hz. The stimulation had no effect on the c-fos inducibility at 2 days postinjury.

Animals↗

Trigeminal primary projection to the rat brain stem sensory trigeminal nuclear complex and surrounding structures revealed by anterograde transport of cholera toxin B subunit-conjugated and Bandeiraea simplicifolia isolectin B4-conjugated horseradish peroxidase.

Trigeminal primary afferent neurons were labeled by injecting the rat trigeminal ganglion with either wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP), cholera toxin B subunit (B)-HRP or Bandeiraea simplicifolia isolectin B4 (IB4)-HRP. B-HRP stained medium to large cells (> 600 microm2), while IB4-HRP mostly small cells (< 400 microm2). WGA-HRP labeled trigeminal ganglion neurons of all sizes. Cell bodies in the mesencephalic trigeminal tract nucleus were labeled with WGA-HRP and B-HRP but not IB4-HRP. B-HRP revealed dense projection to the entire brain stem sensory trigeminal nuclear complex (BSTC) except for lamina II of the medullary dorsal horn (MDH). Some contralateral projection was also seen in the caudal part of MDH. Non-trigeminal nuclei receiving B-HRP-labeled terminals included the paratrigeminal nucleus (paraV), solitary tract nucleus, supratrigeminal nucleus, Probst's nucleus and median accessory nucleus. Following IB4-HRP application, terminal label was found in more restricted regions within the BSTC. Modest terminal label was seen in the dorsal part of principal sensory nucleus and at the medial edge of subnucleus interpolaris, while relatively dense terminal fields were seen in the dorsal half of subnucleus oralis. The MDH laminae I and II contained dense terminal label. Non-trigeminal nuclei were almost devoid of the IB4-HRP-labeled terminals excepting the paraV that contained dense terminal label. The terminal areas revealed with WGA-HRP coincided with B-HRP-labeled and IB4-HRP-labeled areas combined.

Animals↗

Neurochemistry of the nodose ganglion.

Placode-derived general visceral afferent neurons of the nodose ganglion transmit visceral sensory information from specialized sensory endings of the vagus nerve and its branches to the nucleus of the solitary tract. These neurons are critical in relaying information such as elevations in blood pressure, changes in blood oxygenation, passage of contents through the esophagus and intestines, and distention of the heart, stomach, and lungs to the CNS for reflex maintenance of visceral functions. Multiple neurotransmitters, neuropeptides, calcium binding proteins, and other neuroactive substances are associated with neurons of the nodose ganglion. Many neurons colocalize 2 or more neuroactive substances creating the potential for complex interactions of neurochemical signals in the NTS. Neurons of the nodose ganglion also contain a variety of receptors which respond to transmitters, inflammatory mediators, and neurotrophic factors. The contents of these neurochemicals and receptors are not static as alterations in their expression are noted in response to epigenetic influences. Although not yet well understood, potential factors and mechanisms regulating neurochemical events in the nodose ganglion neurons are discussed.

Animals↗

Role of lipid peroxidation and antioxidants in gastric mucosal injury induced by the hypoxanthine-xanthine oxidase system in rats.

Free radical-induced gastric mucosal injury was caused by severe depletion of glutathione and alpha-tocopherol. Intravenous infusion of hypoxanthine (HX) via the jugular vein and local intra-arterial infusion of xanthine oxidase (XO) via the left gastric artery caused marked gastric mucosal injury in the antrum and the corpus. This study was performed to determine whether antioxidants in the gastric mucosa are mobilized during oxidative stress in the rat stomach. The level of thiobarbituric acid (TBA) reactive substance in the gastric mucosa was not significantly changed. The levels of total glutathione and alpha-tocopherol in the gastric mucosa significantly decreased. Total superoxide dismutase (Cu/Zn-and Mn-SOD) and glutathione peroxidase activities were not significantly changed. Administration of SOD reversed the glutathione level but not the alpha-tocopherol level in the gastric mucosa. To determine the role of glutathione and alpha-tocopherol in oxidative stress, the stomach was removed from a normal, alpha-tocopherol supplemented, and glutathione-depleted rat and used for experimentation. Frozen slices of the rat stomach were infused with HX-XO then examined histochemically using cold Schiff's reagent for signs of lipid peroxidation. It was found that the alpha-tocopherol supplemented stomach inhibited lipid peroxidation induced by HX-XO. Biochemical measurements and histochemical examination showed that the glutathione-depleted frozen tissue section and the homogenate had increased by lipid peroxidation induced by HX-XO. These findings suggested that alpha-tocopherol and glutathione may play a role in protecting the gastric mucosa against oxygen free radicals.

Animals↗

Characterization of an interleukin 1 receptor antagonist protein released from ultraviolet-irradiated epidermal sheet.

An interleukin 1 (IL-1) inhibitor was detected in the culture supernatant of mouse epidermal sheet which had been irradiated with middle-wavelength ultraviolet (UVB) either in vitro or in vivo. Properties of the IL-1 inhibitor were consistent with those of IL-1 receptor antagonist (IL-1ra), i.e., approximate molecular size of 17 kDa by gel filtration, specific inhibition of IL-1-induced thymocyte proliferation, inhibition of binding of IL-1 to IL-1 receptor on the T-cell surface, and reactivity to anti-mouse IL-1ra antibody shown by immunoblotting and enzyme-linked immunosorbent assay (ELISA). These results indicate that this IL-1 inhibitor, which appears to be identical with IL-1ra, was released from the epidermis upon UVB irradiation, and that the inhibitor may participate in the regulation of inflammation mediated by IL-1, as well as in the pathogenesis of ultraviolet (UV)-induced immunosuppression.

Animals↗