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Biomedical subjects

H Iizuka

Publications and source records attributed to H Iizuka.

At least 37 records · Page 2Linked to original sources
PubMed2001

Nuclear localization of beta-catenin in the hair matrix cells and differentiated keratinocytes.

Beta-catenin is a structural component of adherens junctions and also a downstream effector of Wnt signaling pathway. Beta-catenin has been detected in the adherens junctions in almost all normal tissues including the epidermis. Only in some malignant tumor cells was it found in the cytoplasm and nuclei. Recently pilomatricoma was found to be caused by mutations of amino-terminal segment of beta-catenin, normally involved in phosphorylation-dependent ubiquitin-mediated degradation of the protein. Since nuclear beta-catenin has not been detected in pilomatricoma or any other benign follicular tumors, we investigated localization of beta-catenin in the normal hair follicle, follicular tumor cells, normal and psoriatic epidermis by using immunohistochemical method with a high temperature antigen unmasking technique. The nuclear localization of beta-catenin was detected not only in the matrix cells of follicular tumors including pilomatricoma but also in the normal hair matrix cells and the differentiated keratinocytes of the upper layers of the epidermis. Cell membrane staining of beta-catenin and E-cadherin was decreased in these differentiated keratinocytes. This coincided with the emergence of nuclear beta-catenin. The present immunohistochemical method has revealed hitherto unproven nuclear localization of beta-catenin in hair matrix cells. Our results also provided evidence suggesting that beta-catenin plays an important role in keratinocyte differentiation.

Cell Differentiation↗
PubMed2001

Corneodesmosin expression in psoriasis vulgaris differs from normal skin and other inflammatory skin disorders.

SUMMARY: Corneodesmosin (Cdsn) is a late differentiation epidermal glycoprotein putatively involved in keratinocyte adhesion. The Cdsn gene lies within the susceptibility region on chromosome 6p21.3 (PSORS1) for psoriasis, a common chronic disfiguring skin disease. A particular allelic variant of Cdsn has a strong association with psoriasis. Therefore, genetically and biologically, Cdsn is a possible candidate gene for psoriasis susceptibility. To investigate a potential role for Cdsn in psoriasis pathogenesis, protein expression studies were performed by quantitative immunohistochemistry on normal skin, psoriatic skin (lesional and nonlesional), and other skin disorders using monoclonal antibodies (G36-19 and F28-27). In normal and nonlesional skin, Cdsn was expressed in stratum corneum and one or two layers of superficial stratum granulosum. In lesional psoriasis, there was a significant increase in Cdsn expression, which was observed in multiple layers of stratum spinosum and in stratum corneum. The expression pattern varied from granular, cytoplasmic immunoreactivity to cell surface labeling with weakly immunoreactive cytoplasm. In chronic atopic dermatitis, lichen planus, mycosis fungoides, and pityriasis rubra pilaris, Cdsn immunoreactivity was confined to stratum corneum and upper stratum granulosum with no stratum spinosum immunoreactivity. Immunoelectron microscopy of normal and lesional psoriatic skin demonstrated Cdsn release concomitant with involucrin incorporation into cell envelopes and completed before mature envelope formation. Extracellular release of Cdsn occurred at a lower level of the epidermis in psoriasis than normal skin. These protein expression studies provide evidence of altered Cdsn expression in psoriasis consistent with a role of Cdsn in disease pathogenesis. Further functional and genetic studies of Cdsn are justified to determine its role as a potential psoriasis-susceptibility factor.

Chromosomes, Human, Pair 6↗
PubMed2001

Effect of oesophagectomy on monocyte-induced apoptosis of peripheral blood T lymphocytes.

BACKGROUND: Surgical stress has been reported to induce immunosuppression. The mechanisms giving rise to T-cell dysfunction following surgery are still unclear. The cellular mechanisms behind T-cell dysfunction following surgery were investigated, based on the induction of T-cell apoptosis and downregulation of T-cell signalling molecules. METHODS: Peripheral blood T cells were collected and separated before and after surgery in patients who had oesophagectomy, gastrectomy or cholecystectomy, and studied for their ability to produce cytokines, the induction of T-cell apoptosis with terminal deoxynucleotidyl transferase-mediated dUPT-biotin nick end labelling methods, and the expression of T-cell signalling zeta (TCR zeta) molecules with intracellular staining. RESULTS: The increased degree of T-cell apoptosis, downregulation of TCR zeta molecules and impaired cytokine production of T cells were significant on days 1 and 3 after operation in patients who had oesophagectomy, but not after gastrectomy or cholecystectomy. A higher level of T-cell apoptosis was observed in the co-culture with postoperative monocytes than with preoperative monocytes. CONCLUSION: Peripheral blood T cells obtained after oesophagectomy underwent apoptosis that correlated with the downregulation of TCR zeta molecules. Postoperative monocytes induced by surgical stress were able to mediate the T-cell apoptosis.

Aged↗
PubMed2001

Ultraviolet B irradiation induces apoptosis of keratinocytes by direct activation of Fas antigen.

Ultraviolet B (UVB) irradiation induces apoptosis of keratinocytes, where p53 has been suggested to play an important role. Recently we have shown that UVB irradiation induces apoptosis of SV40-transformed human keratinocytes (SVHK cells). Because p53 function is impaired in SVHK cells by large T antigen, a UVB-induced p53-independent apoptotic pathway was suggested. We investigated the UVB-induced apoptotic pathway using various keratinocytes. Cultured mouse keratinocytes of homozygous p53 deficient mice (p53(-/-)) were markedly resistant to UVB-induced apoptosis compared with keratinocytes from wild or heterozygous p53 deficient mice (p53(-/+)). Twenty per cent of keratinocytes derived from p53 (-/-) mice, however, induced apoptosis following UVB irradiation. Analysis using caspase inhibitors disclosed activation of caspase 8 and 3 in UVB-irradiated SVHK cells. Keratinocytes derived from MRL/lpr mice, which have mutated Fas antigen, showed diminished UVB-induced apoptosis suggesting that Fas antigen is significantly involved in UVB-induced apoptosis. Immunohistochemical analysis revealed that UVB irradiation induces aggregation of Fas antigen showing a dense dot-like staining, which was also observed in SVHK cells treated with agonistic anti-Fas antibody, CH11. Pretreatment of antagonistic anti-Fas antibody, ZB4, inhibited CH11-induced but not UVB-induced multimerization of Fas antigen. Furthemore, UVB irradiation did not affect the basal expression of Fas ligand mRNA, protein and soluble Fas ligand. These results indicate that UVB irradiation induces multimerization of Fas antigen that results in apoptosis without the Fas ligand.

Animals↗
PubMed2001

Loricrin keratoderma: a cause of congenital ichthyosiform erythroderma and collodion baby.

A group of hereditary palmoplantar keratodermas due to heterozygous mutation in the loricrin gene has recently been identified. Of five reported pedigrees, four presented as mutilating keratoderma with ichthyosis (variant Vohwinkel syndrome), and one as progressive symmetric erythrokeratoderma. We report a new Japanese pedigree of loricrin keratoderma. A 14-year-old male and his 11-year-old female sibling had both been born as collodion babies and were initially diagnosed as having non-bullous congenital ichthyosiform erythroderma, but later developed palmoplantar keratoderma with pseudoainhum. Their father was similarly affected. Direct sequencing of genomic DNA revealed a G residue insertion at codon 230-231 of the loricrin gene. Antibody studies confirmed the presence of mutant loricrin in the retained nuclei. We conclude that loricrin gene mutation may present as congenital ichthyosiform erythroderma, and should be included in the differential diagnosis of collodion baby.

Adolescent↗
PubMed2001

Syringocystadenocarcinoma papilliferum: case report and immunohistochemical comparison with its benign counterpart.

Syringocystadenocarcinoma papilliferum (SCACP) is the malignant counterpart of syringocystadenoma papilliferum (SCAP), although only a few cases have been reported in the literature and its clinical and histologic characteristics are not well known. We report a case of SCACP that started as an enlarging nodule over 10 years in the perianal area of a 61-year-old man. Macroscopically, the lesion was a black exophytic tumor, 6 cm in diameter, with a granular surface. Histologically, it was an in situ adenocarcinoma, showing cytologic atypia and pagetoid spread in the surrounding epithelia, although the clinicopathologic features were distinct from extramammary Paget's disease. The tumor lacked the typical double-layered pattern of SCAP but had some similar histopathologic features to SCAP. Decapitation secretion was apparent and there was positive immunoreactivity to epithelial membrane antigen and human milk fat globules subclass 2. SCACP is a rare cutaneous tumor but nevertheless represents a specific dermatopathologic entity.

Adenocarcinoma↗
PubMed2001

Interposed colon between remnants of the small intestine exhibits small bowel features in a patient with short bowel syndrome.

We describe herein the case of a 48-year-old man who underwent emergency massive resection of the small intestine due to a strangulated ileus, which led to short bowel syndrome (SBS), as he was left with only 7 cm of jejunum and 8 cm of ileum with ileocecal valve. He then received interposition of a colon segment between the jejunum and ileum remnants isoperistaltically. For 24 months after the operation, he has been able to tolerate oral intake, but still requires partial home parenteral nutritional support during the night on a bimonthly basis. Biochemical and nutritional parameters, including the analysis of minerals and trace elements, indicated that the patient was in relatively good health. Histological examination revealed that the mucosa of the interposed colon showed hypertrophy and hyperplasia of the crypt glands, and cells resembling Paneth cells which are usually seen in the small intestine, suggesting that the colon segment exhibits adaptive changes to the small intestine. Colon interposition may be a useful technique in patients with SBS when the small bowel is too short for the other surgical considerations.

Anastomosis, Surgical↗
PubMed2001

Pigmented Paget's disease of the male breast: report of a case.

An 83-year-old man with pigmented Paget's disease of the breast is reported. He had a blackish swollen right nipple with bloody discharge that lasted for 8 months. Histopathology of the lesion disclosed intraepidermal and dermal atypical cells forming small clusters and underlying intraductal carcinoma. Melanocytes were dispersed in the epidermis. Dermal melanophages were also detected. The atypical cells were positive for carcinoembryonic antigen, human-milk fat globule protein and a recently described new antigen, RCAS-1, but negative for S-100 or HMB-45. We diagnosed this case as Paget's disease of the male breast. Paget's disease of the breast is usually nonpigmented and occurs almost exclusively in women. Pigmented Paget's disease of the male breast is extremely rare, and only a few cases have been reported. Albeit rare, pigmented Paget's disease has to be included in the differential diagnosis of pigmented lesions of the nipple.

Aged↗
PubMed2001

In vitro and in vivo transfer of bcl-2 gene into keratinocytes suppresses UVB-induced apoptosis.

Bcl-2 is a member of the large Bcl-2 family and protects cells from apoptosis. Ultraviolet B (UVB) irradiation induces apoptosis of keratinocytes that is known as "sunburn cells." Previously we reported that UVB irradiation induces apoptosis accompanied by sequential activation of caspase 8, 3 and 1 in keratinocytes, and that the process is inhibited by various caspase inhibitors. Using bcl-2-expressing adenovirus vector we investigated the effect of Bcl-2 on UVB-induced apoptosis. Adenovirus vector efficiently introduced bcl-2 gene in cultured normal mouse keratinocytes (NMK cells); almost all NMK cells (1 x 10(6)) were transfected at 1 x 10(8) plaque-forming unit (PFU)/mL. Bcl-2-transfected NMK cells were significantly resistant to UVB-induced apoptosis with the suppressive effect dependent on the Bcl-2 expression level. Following UVB irradiation caspase 8, 3 and 9 activities were stimulated in NMK cells, whereas in bcl-2-transfected cells only caspase 8, but not caspase 3 or 9, activity was stimulated. In order to investigate the effect of Bcl-2 in vivo topical application of Ad-bcl-2 on tape-stripped mouse skin was performed. Following the application Bcl-2 was efficiently overexpressed in almost all viable keratinocytes. The expression was transient with the maximal expression of Bcl-2 on the first day following the application of 1 x 10(9) PFU in 200 microL. The introduced Bcl-2 remained at least for 6 days. UVB irradiation (1250 J/m2) induced apoptosis within 12 h and the maximal effect was observed at 24 h in control mouse skin. Both bcl-2-transfected and topical caspase 3 inhibitor-treated mice skin were resistant to UVB-induced apoptosis. The suppressive effect of Bcl-2 was more potent than that of caspase 3 inhibitor application. Topical application of empty adenovirus vector alone had no effect on Bcl-2 expression or UVB-induced apoptosis. These results indicate that adenovirus vector is an efficient gene delivery system into keratinocytes and that Bcl-2 is a potent inhibitor of UVB-induced apoptosis both in vitro and in vivo.

Adenoviridae↗
PubMed2001

Elevated caspase-3 activity in peripheral blood T cells coexists with increased degree of T-cell apoptosis and down-regulation of TCR zeta molecules in patients with gastric cancer.

To evaluate the mechanisms of T-cell dysfunction in patients with gastric cancer, we investigated the caspase activity of T cells, the induction of spontaneous T-cell apoptosis, the expression of T-cell receptor (TCR) zeta molecules, and the ability of T cells to produce cytokines in peripheral blood lymphocytes from patients (n = 22) and healthy controls (n = 14). The caspase-3 activity of T cells was studied as the protease activity of caspase-3 using the cell-permeable substrate of PhiPhiLux G1D2. Flow cytometric analysis was performed with triple staining by annexin V-FITC, propidium iodide, and CD3-R-phycoerythrin-Cy5 for the detection of T-cell apoptosis and with intracellular staining using permeabilized cells for the expression of TCR-zeta molecules. IFN-gamma and tumor necrosis factor alpha production from T cells was evaluated in response to anti-CD3 stimulation. Caspase-3 activity of peripheral blood T cells from patients with advanced disease was significantly increased compared with that from controls [15.5 +/- 3.6 mean fluorescence intensity (MFI) versus 11.5 +/- 3.3 MFI; P = 0.0068]. Parallel to this, the apoptosis of peripheral blood T cells from patients with advanced disease was significantly higher than for those from controls (16.5 +/- 15.5% versus 4.8 +/- 2.7%; P = 0.010). Furthermore, the expression of TCR-zeta molecules in patients with advanced disease was significantly decreased in comparison with that of the controls (41.0 +/- 13.9 MFI versus 56.7 +/- 16.3 MFI; P = 0.014), and this decreased expression coexisted with impaired IFN-gamma (42.4 +/- 43.2 pg/ml versus 1,757.4 +/- 2449.0 pg/ml; P = 0.031) and tumor necrosis factor alpha (682.6 +/- 519.3 pg/ml versus 1,686.0 +/- 1,533.7 pg/ml; P = 0.041) production of T cells. Thus, peripheral blood T cells from gastric cancer patients simultaneously exhibit an elevated caspase-3 activity, an increased degree of T-cell apoptosis, a down-regulation of TCR-zeta molecules, and impaired cytokine production. These observations suggest that induction of T-cell apoptosis coexisting with a down-regulation of TCR-zeta molecules may be responsible for T-cell dysfunction in patients with gastric cancer.

Apoptosis↗
PubMed2001

[A case of central nervous system anomalies (agenesis of corpus callosum, colpocephaly, hydrocephalus, congenital dermal sinus) associated with congenital heart disease(double-outlet right ventricle, complete endocardial cushion defect, atrial septal defect, pulmonary arterial stenosis, patent ductus arteriosus)].

A case of central nervous system anomalies(agenesis of corpus callosum, colpocephaly, hydrocephalus, congenital dermal sinus) associated with congenital heart disease(double-outlet right ventricle, complete endocardial cushion defect, atrial septal defect, pulmonary arterial stenosis, patent ductus arteriosus) is reported. Female patient had been already diagnosed as hydrocephalus during pregnancy and ventricular drainage was performed soon after the delivery. Prostaglandin E 1 was also applied for heart disease, but saturation of O2 decreased to 80% on arterial blood gas analysis. Blalock-Taussig operation and ligation of ductus arteriosus was done 41 days after the delivery and ventricle-peritoneal shunt was also made for the progressive hydrocephalus on the same day. Chromosome analysis showed no abnormality. The genesis of this complicated brain and heart anomaly is discussed from the viewpoint of neural crest cell abnormality.

Abnormalities, Multiple↗
PubMed2001

[Memory disturbance caused by medial temporal lesion].

The memory disturbance caused by medial temporal lesion is reported concerning 6 cases of cerebral hemorrhage, infarction, brain tumor, and contusion. The memory disturbance was significant compared with the patient's intact orientation and normal intelligence. In the category of memory, recent memory was more markedly disturbed than the immediate or remote memory. From the viewpoint of the lesion, the memory disturbance was more severe when, in addition to the hippocampus, the entorhinal gyrus or amygdala was damaged. The visual memory disturbance was mild and no difference was observed in the verbal or visual memory according to whether the lesion was right or left. The memory disturbance was usually transient and marked improvement was observed in some cases.

Adult↗
PubMed2001

[A case of cardiac myxoma with multiple brain hemorrhage].

A case of cardiac myxoma with multiple brain hemorrhage is reported. A 57-year-old male had complained of lower abdominal pain, diarrhea and fever for 3 days. On admission, he was in a condition of disseminated intravascular coagulation and sepsis. An abdominal CT scan showed infarction in the right kidney and spleen and an echocardiogram also showed myxoma in the left atrium. Although he presented no neurological symptoms, the brain CT showed multiple brain hemorrhage in the bilateral brain hemispheres. Total resection of the tumor was carried out for the improvement of the patient's general condition. Vimentin, S-100 protein and neuron specific enolase was positive in immunological staining and the pathological diagnosis was myxoma. Postoperative recovery of consciousness was poor and left hemiparesis developed. CT showed the increase of hematoma but angiography showed no cerebral aneurysm. The symptoms improved with conservative therapy. However the enhanced lesion remained in the right parietal lobe and an operation was performed 5 months later. The myxoma cell could not be found in the pathological examination, so tumor embolism, cerebral infarction, hemorrhagic infarction due to DIC, hematoma enlargement caused by heparinization during operation were suspected to have occurred in this order without tumor growth.

Brain↗
PubMed2000

Transcriptional factor AP-2gamma increases human cystatin A gene transcription of keratinocytes.

The transcriptional activator protein-2 (AP-2) has been suggested to participate in keratinocyte gene regulation. Cystatin A, a cysteine proteinase inhibitor, is one of the cornified cell envelope constituents and is expressed in the upper epidermis. We report AP-2-dependent transcriptional regulation of cystatin A gene expression of keratinocytes. At least three isoforms of AP-2 (AP-2 alpha, beta, gamma) have been described. Transfection of AP-2alpha, beta and gamma expression vectors into cultured normal human keratinocytes (NHK) resulted in increased cystatin A expression in both mRNA and protein levels. Among the three isoforms AP-2gamma was most potent in inducing cystatin A expression. In contrast, transfection of antisense oriented AP-2gamma expression vector decreased basal AP-2 expression, accompanied by decreased cystatin A mRNA. The fragment, +77 to -478 of 5'-flanking region of human cystatin A gene, was subcloned into chloramphenicol acetyltransferase (CAT) reporter vector (p478CAT). Cotransfection of p478CAT vector with AP-2alpha, beta, and gamma expression vectors resulted in three-, three-, and sixfold increase in the CAT activity, respectively. Transfection of the deleted construct (p478DeltaAP-2CAT, devoid of AP-2-like binding site (-75 to -84)) decreased CAT activity by one-third compared to p478CAT promoter activity. Cotransfection of p478DeltaAP-2CAT with AP-2alpha, beta, and gamma expression vectors had no effect on the decreased promoter activity. Immunohistochemical analysis of human skin showed that AP-2alpha is exclusively expressed in the nuclei of basal cell layer. AP-2gamma is expressed in the nuclei of basal, spinous, and granular cell layers. AP-2beta expression was not observed in the epidermis. Gel mobility shift assay revealed that the AP-2gamma protein specifically binds to oligonucleotides containing AP-2-like binding site of cystatin A gene. These results indicate that AP-2gamma regulates the cystatin A gene expression of epidermal keratinocytes at the transcriptional level.

5' Untranslated Regions↗
PubMed2000

Involvement of receptor activator of nuclear factor kappaB ligand/osteoclast differentiation factor in osteoclastogenesis from synoviocytes in rheumatoid arthritis.

OBJECTIVE: To clarify the mechanism by which osteoclasts are formed in culture of rheumatoid synoviocytes by exploring the involvement of receptor activator of nuclear factor kappaB ligand (RANKL)/osteoclast differentiation factor (ODF). METHODS: Osteoclast formation was evaluated in cocultures of rheumatoid synovial fibroblasts and peripheral blood mononuclear cells (PBMC) in the presence of macrophage colony stimulating factor and 1,25-dihydroxyvitamin D3 (1,25[OH]2D3) utilizing separating membrane filters. RANKL/ODF expression was examined by Northern blotting in synovial tissues from 5 rheumatoid arthritis (RA) patients and tissues from patients with giant cell tumor (GCT), osteosarcoma (OS), and osteoarthritis (OA). RANKL/ODF expression and the ability of synovial fibroblasts to support osteoclastogenesis were investigated in coculture with PBMC in the presence or absence of 1,25(OH)2D3, and soluble RANKL/ODF and osteoprotegerin (OPG)/osteoclastogenesis inhibitory factor (OCIF) were measured by enzyme-linked immunosorbent assay. The effects of OPG/OCIF on the osteoclastogenesis in the primary culture of rheumatoid synoviocytes and the coculture system were determined. RESULTS: Synovial fibroblasts did not induce osteoclastogenesis when separately cocultured with PBMC. Northern blotting revealed that RANKL/ODF was highly expressed in all tissues from RA and GCT patients, but not from OA or OS patients. Cultured rheumatoid synovial fibroblasts efficiently induced osteoclastogenesis in the presence of 1,25(OH)2D3, which was accompanied by up-regulated expression of RANKL/ODF and decreased production of OPG/OCIF. Osteoclastogenesis from synoviocytes was dose-dependently inhibited by OPG/OCIF. CONCLUSION: RANKL/ODF expressed on synovial fibroblasts is involved in rheumatoid bone destruction by inducing osteoclastogenesis and would therefore be a good therapeutic target.

Arthritis, Rheumatoid↗
PubMed2000

The entire nucleotide sequences of two distinct TT virus (TTV) isolates (TJN01 and TJN02) remotely related to the original TTV isolates.

TT virus (TTV) has a wide range of sequence divergence by which it is classified into at least 16 genotypes. A TTV isolate of genotype 12 (TJNO1) and another of genotype 13 (TJN02) were sequenced in the entire genome, and compared with the reported TTV isolates. TJN01 and TJN02 had genomic lengths of 3787 and 3794 nucleotides (nt), respectively, which were shorter by 66 and 59 nt than the prototype TTV isolate of genotype 1 (TA278). TJN01 and TJN02 shared the nucleotide sequence with TA278 merely in 53.9% and 55.2%, respectively. They possessed two major open reading frames (ORFs) and the noncoding region with a GC-rich region forming stem-loop structures, which are characteristic of TTV. However, their amino acid sequences in ORF1 were similar to that of TA278 in only 35.4 and 34.0%, respectively; TJN01 was 45.4% similar to TJN02. Comparison with TTV isolates of the same genotype identified hypervariable regions in ORF1 of TJN01 and TJN02, as in the prototype TTV of genotype 1. However, quasispecies were barely observed in them. Furthermore, sequences of hypervariable regions scarcely changed during 2-5.5 years in both TJN01 and TJN02. These results indicate that TTV of genotypes 12 and 13 are much different from the prototype TTV of genotype 1.

Adolescent↗
PubMed2000

Cornified cell envelope formation is distinct from apoptosis in epidermal keratinocytes.

In order to maintain epidermal structural homeostasis, keratinocytes need to modulate their proliferation, differentiation, and cell death. Although terminal differentiation of keratinocytes is characterized by cornified cell envelope (CE) formation and one major mechanism of cell death is apoptosis, the precise relationship between these processes remains obscure. Using normal human cultured keratinocytes (NHK), we compared A23187-induced CE formation and ultraviolet B irradiation (UVB)-induced apoptosis. A23187 stimulated CE formation in 1 mM Ca(2+)-pretreated NHK cells. CE formation was detected by 1 h and the maximal induction was observed at 6 h. Morphological analysis using acridine orange staining revealed that UVB-irradiated NHK cells show distinctive round, homogeneous fragmented nuclear beads, a characteristic feature of apoptotic cells, while A23187-treated cells showed enlarged nuclei with weak chromatin staining, which is not typical of apoptosis. The UVB-irradiated NHK cells did not show CE formation. Caspase activation is a characteristic event during apoptosis. Although UVB irradiation increased caspase 3 activity, no increase in caspase 3 activity was detected during A23187-induced CE formation. Multiple nucleosome-sized fragments of DNA were observed in UVB-treated NHK cells, but not in A23187-treated NHK cells. FACS analyses using anti-annexin V antibody and propidium iodide (PI) showed that UVB irradiation induced both annexin V-positive and PI-negative early apoptotic cells and annexin V-positive and PI-positive late apoptotic cells. On the other hand, A23187-treated NHK cells showed only annexin V-negative and PI-positive non-apoptotic dying cells. Cell death assay revealed a significantly increased apoptotic cells in UVB-irradiated NHK cells, but not in A23187-treated NHK cells. UVB irradiated NHK cells showed increased cytosolic transglutaminase activity, while A23187-treated NHK cells showed increased membrane-associated transglutaminase activity. These results indicate that CE formation is distinct from apoptosis in epidermal keratinocytes.

Anti-Bacterial Agents↗