[Changes of hair papilla and its role in the growth cycle of the hair follicles].

OBJECTIVE: To investigate the changes of hair dermal papilla and its regulatory role in the growth cycle of the hair follicles. METHODS: Single hair follicles were isolated from surgical specimens of human scalp and cultured in Williams E medium. The growth of the hair follicle was measured and the morphology and structure of the dermal papilla in the different growth cycles were observed continuously. RESULTS: The hair follicle could grow in the medium for 12 days at the average growth rate of 0.2-0.3 mm/day. The flat and round dermal papilla lay at the bottom of the hair bulb in the telogen and anagen stages. In the hair follicle with accelerated growth, the dermal papilla became elongated, loosened, and closely adhered to the hair matrix. In the catagen stage the dermal papilla shrunk, and became separated from the hair matrix. A new hair bulb was regenerated when the hair follicle was transected at a low level. The hair follicle stopped growing after transection at a higher position. CONCLUSION: The hair dermal papilla is the essential for hair follicle growth, and plays an important role in regulating the hair growth cycle.

Angiotensin II regulates phosphoinositide 3 kinase/Akt cascade via a negative crosstalk between AT1 and AT2 receptors in skin fibroblasts of human hypertrophic scars.

Angiotensin II (Ang II) stimulation has been shown to regulate proliferation of skin fibroblasts and production of extracellular matrix, which are very important process in skin wound healing and scarring; however, the signaling pathways involved in this process, especially in humans, are less explored. In the present study, we used skin fibroblasts of human hypertrophic scar, which expressed both AT1 and AT2 receptors, and observed that Ang II increased Akt phosphorylation and phosphoinositide 3 kinase (PI 3-K) activity. In addition, the Ang II-induced Akt phosphorylation was blocked by wortmannin, a PI 3-K inhibitor. This Ang II-activated PI 3-K/Akt cascade was markedly inhibited by valsartan, an AT(1) receptor-specific blocker, whereas it was enhanced by PD123319, an AT(2) receptor antagonist. On the other hand, the Ang II- or EGF-induced activation of PI 3-K/Akt was strongly attenuated by AG1478, an inhibitor of epidermal growth factor (EGF) receptor kinase. Moreover, Ang II stimulated tyrosine phosphorylation of EGF receptor and p85alpha subunit of PI 3-K accompanied by an increase in their association, which was inhibited by valsartan, and enhanced by PD123319. The Ang II-induced transactivation of EGF receptor resulted in activation of extracellular signal-regulated kinase (ERK) that was also inhibited by valsartan, and enhanced by PD123319. Taken together, our results showed that AT(1) receptor-mediated activation of PI 3-K/Akt cascades occurs at least partially via the transactivation of EGF receptor, which is under a negative control by AT(2) receptor in hypertrophic scar fibroblasts. These findings contribute to understanding the molecular mechanism of human hypertrophic scar formation.

[Study on corelation between InsP(3) generation and TCR/ CD3 complex-mediated [Ca(2+)]i responses in T cells from SLE patients].

AIM: To demonstrate whether function disorder of T cells from SLE patients was relative to abnormal biochemical pathways mediated by TCR/ CD3 complex and whether this abnormality was relative to the InsP(3) production. METHODS: Human T cells were isolated through Nylon-columns from heparinized peripheral blood from SLE patients and control individuals. Percentage of CD3(+) T cells was detected by flow cytometry. After cross-linking of anti-CD3 mAbs to sheep anti-mouse IgG and stimulating T cells, the changes of free calcium ion within T cells was observed successively for 10 minutes by an adhesion cytometry. Flow cytometry was used to detect the difference in positive rate between normal individual's and SLE patient's T cells. Level of InsP(3) was detected by a radioreceptor assay kit. RESULTS: (1)Flow cytometry analysis showed that CD3(+) T cells obtained through nylon column accounted for more than 90%.(2)The base line recordings of [Ca(2+)]i response from SLE patients were similar to that from normal control (P=0.105). Peak and plateau [Ca(2+)]i response in T cells of SLE patients were significantly higher than that in the control group (P<0.001). (3)The percentage of the CD3(+) T cells was similar in both individuals (P=0.665).(4)No differences in the anti-CD3 mAb-mediated InsP(3) generation were found between the two groups (P=0.537). CONCLUSION: TCR/ CD3-mediated [Ca(2+)]i responses in T cells from SLE patients is abnormal, and the abnormality has no relation to InsP(3) generation.

Analysis of clinical and immunological features of patients with systemic lupus erythematosus complicated by hepatitis C virus infection.

OBJECTIVE: To investigate the prevalence and clinical significance of hepatitis C virus (HCV) infection in patients with systemic lupus erythematosus (SLE). METHODS: Serodiagnosis was conducted in 134 SLE patients and 200 volunteer blood donors to examine the antibodies of HCV with enzyme-linked immunosorbent assay-3 (ELISA-3). Recombinant immunoblot assay-3 (RIBA-3) and PCR were performed to verify the results. RESULTS: HCV infection was present in 15 patients with SLE (11.8%) and in 2 volunteer donors (1%, P<0.001). Compared with the SLE patients without HCV infection, the patients with HCV infection had a lower rate of cutaneous SLE features and dsDNA positivity (P=0.01 and P<0.001), but with higher incidences of hepatic damage (P<0.001) and low levels of C4 and CH50 (P=0.01 and P=0.03) as well as cryoglobulins levels (P=0.03). CONCLUSION: The prevalence of HCV infection is higher in SLE patients than in non-SLE subjects, and SLE patients with positive HCV show a lower rate to present cutaneous SLE features and positive dsDNA antibody, but who have higher possibilities of hepatic damage, hypocomplementemia and cryglobulinemia.