Therapeutic Effects of Growth Factor Cocktail Including Fibroblast Growth Factor 9 in Patients with Pattern Hair Loss / 대한피부과학회지

BACKGROUND: A growth factor cocktail (GFC) including fibroblast growth factor 9 (FGF9) in combination with microneedling is an effective and safe treatment for patients with androgenetic alopecia (AGA). However, there is a lack of studies evaluating its effects based on microneedle depth. OBJECTIVE: This study aimed to evaluate the effects of a GFC including FGF9 on hair growth in patients with AGA, and compare the differences in efficacy according to microneedle depth. METHODS: The study was performed on patients with AGA who were treated with topical GFC including FGF9 with microneedling once every 2 weeks for 3 months. The scalp was divided into right and left sides, and treated with GFC including FGF9 (right side) and normal saline (left side). The microneedle depth was 0.8 mm for both sides. A total of 22 patients (11 males and 11 females) were enrolled. GFC including FGF9 was topically applied with a microneedle medical device. Treatment efficacy was evaluated through phototrichogram and digital photograph analyses after 6 repeated treatments for 3 months. RESULTS: The phototrichogram images showed that 3 months of treatment with GFC including FGF9 with microneedling increased hair density (27.4±4.4/cm²) and diameter (2.7±2.7 µm); increases in hair density (5.7±4.4/cm²) and diameter (2.2±2.3 µm) were also seen in the region of the scalp that received normal saline. These results were statistically significant (p < 0.05). The treatment effect was not significantly different between microneedle depths of 0.8 mm (used in this study) and 0.5 mm (used in our previous study) in terms of both hair density and hair diameter. CONCLUSION: GFC including FGF9 with microneedling is an effective and safe treatment for patients with AGA. According to the results of this study and our previous report, we believe that microneedle depths of 0.5∼0.8 mm can sufficiently stimulate the scalp to increase drug-delivery.

Clinical study of inflammatory factors in sputum induced early after lung volume reduction surgery / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The aim of this study was to prospectively study the changes in neutrophil elastase (NE), fibroblast growth factor 9 (Fgf9), matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase 1 (TIMP-1) in sputum induced during the early period after lung volume reduction surgery (LVRS).</p><p><b>METHODS</b>From April to October 2005, ten consecutive patients with chronic obstructive pulmonary disease (COPD) underwent LVRS. Ten non-small cell lung cancer patients (stage II - IIIa) received lobectomy as a control group. The induced sputum was collected from both groups at six different times (two weeks before operation and postoperatively at 1, 2, 4, 6 and 10 days). The level of NE, Fgf9, MMP-9 and TIMP-1 were measured using enzyme-linked immunosorbent assay.</p><p><b>RESULTS</b>The pulmonary function (FEV(1)%) and arterial blood gases (PaO(2) and PaCO(2)) were significantly different between the groups. There were no significant differences in age, ejection fraction (EF), and operation duration, but hemoglobin in the LVRS group was statistically higher than in the controls. At certain times, there were significant differences in NE, MMP-9, TIMP-1 and MMP-9/TIMP-1 (P < 0.05) but not in Fgf9 between the two groups. The levels of NE and TIMP-1 were maximal at 2 days postoperatively and that of MMP-9 and MMP-9/TIMP-1 at 4 days postoperatively in the LVRS group. In the control group, maximal levels of NE and TIMP-1 occurred at 2 days postoperatively and that of MMP-9 and MMP-9/TIMP-1 at 1 day postoperatively. Ten days after surgery, all values of the control group were not significantly different from the baseline. In the LVRS group, the levels were significantly different from the pre-operative values (P < 0.05) apart from TIMP-1.</p><p><b>CONCLUSION</b>The levels of NE, MMP-9, TIMP-1 and MMP-9/TIMP-1 of the LVRS group were different from those of the control group. The time course of these changes may be related to LVRS and the underlying process of COPD.</p>

Effect of fibroblast growth factor 9 on Runx2 gene promoter activity in MC3T3-E1 and C2C12 cells / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Fibroblast growth factor 9 (FGF9), expressed in brain, kidney and developing skeletal tissues, can physiologically inhibit endochondral ossification; but little is known about how FGF9 affects osteoblasts and its detailed regulatory mechanism. Here we examined the effect of FGF9 on the activity of the murine Runt-related transcription factor 2 (Runx2) gene promoter in preosteoblast MC3T3-E1 and premyoblast C2C12 cells.</p><p><b>METHODS</b>Plasmids containing the Runx2 promoter region were transfected into MC3T3-E1 and C2C12 cells and stably transfected cell lines were established. The method of luciferase reporter gene activation was used to examine the effects of FGF9 on the promoter activity.</p><p><b>RESULTS</b>FGF9 (10 ng/ml) increased Runx2 promoter activity in MC3T3-E1 cells. When MC3T3-E1 cells were treated with FGF9 plus the various inhibitors or activator of the intracellular signaling transducation pathways, including 10 micromol/L U0126 (the inhibitor of mitogen-activated protein kinase kinase), 10 micromol/L SB203580 (the inhibitor of p38/mitogen activated protein kinase), or 1 micromol/L C6 ceramide (an activator of mitogen activated protein kinase), the luciferase expression did not change significantly compared with that of the cells treated with FGF9 only. However, when C2C12 cells were treated with 10 ng/ml FGF9, Runx2 gene promoter activity first decreased and then increased over a period of 1 to 5 days. Among the above inhibitors, only U0126 (10 micromol/L) completely blocked the effects of FGF9 on Runx2 gene promoter activity.</p><p><b>CONCLUSIONS</b>Our data showed that FGF9 can affect Runx2 gene promoter activity in MC3T3-E1 and C2C12 cells. The action of FGF9 appears to depend partly on the mitogen-activated protein kinase kinase/mitogen-activated protein kinase pathways in C2C12 cells.</p>