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H Y Park

Publications and source records attributed to H Y Park.

At least 19 recordsLinked to original sources
PubMed2006

Molecular characterization of the porcine endogenous retrovirus subclass A and B envelope gene from pigs.

Xenotransplantation of porcine organs has the potential to overcome the current critical shortage of allogenic organs for transplantation in humans. However, the existence of porcine endogenous retroviruses (PERVs) presents a problem for the clinical use of xenografts from pigs. In an attempt to understand the molecular characteristics of PERVs, we cloned the PERV env gene from six pig breeds (ie, Berkshire, Duroc, Landrace, Yorkshire, and two types of miniature pigs) in Korea. A total of 141 env clones were isolated and their sequences were analyzed. Phylogenetic analyses of these genes revealed the presence of PERVs, from both classes A and B, in 54% and 46% of the env clones, respectively. Among these clones, 37 isolates had the correct open reading frame (ORF; 27 clones in subclass A and 10 clones in subclass B), while the others had premature termination. These PERV nucleotide sequences can be used in a database for comparisons of PERV distribution among different pig breeds and for monitoring PERV infection using isolates with functional ORFs. Recombinant envelope of subclass A and B with functional ORF was expressed by vaccinia virus systems. Additionally isolated env clones can be used for various experiments, such as PERV control and infectivity tests, and may enhance the understanding of molecular mechanisms through pseudotyped PERV viruses.

Animals↗
PubMed2005

Immunochemical and biological analysis of allergenicity with excretory-secretory products of anisakis simplex third stage larva.

BACKGROUND: Anisakis simplex third stage larvae (L3) are parasites that frequently give rise to allergic responses. The larvae molt into fourth stage larvae (L4), and at each stage they produce L3-excretory-secretory products (L3-ESP) and L4-ESP, respectively, which are different in their main protein constituents. Although the allergenicity of L4-ESP has been investigated by several research groups, research on the allergenicity of L3-ESP has not been carried out by any researcher. In this investigation, the allergenicity and antigenicity of L3-ESP were investigated in comparison with L4-ESP, using rat sera. METHODS: Rat sera were produced by L3 oral infection two times with a 9-week interval. Larvae ESP prepared by culture were concentrated and fractioned using lyophilizer and a centrifugal filter device, respectively. Immunochemical analysis was performed using both indirect ELISA and immunoblot. Biological allergenicity was analyzed by RBL-2H3 exocytosis. RESULTS: With the indirect ELISA, the optical density (OD) value of the nonfractioned (NF)-L3ESP was only one third of that of the NF-L4ESP in both specific IgM and IgG. On measuring specific IgE, the OD of NF-L3ESP was less than one tenth of that of NF-L4ESP. In addition, neither antigen nor allergen was shown in NF-L3ESP, but it was shown in NF-L4ESP with immunoblot. However, the biological allergenicity of NF-L3ESP was comparable to that of NF-L4ESP. To demonstrate the presence of any allergen, L3-ESP was fractioned and found to carry twelve visualized allergen bands from 10 to 186 kDa by immunoblot. CONCLUSIONS: These results indicate that L3-ESP may include the important allergens necessary to induce the allergy by L3 oral infection, as compared to L4-ESP.

Allergens↗
PubMed2004

Spatial distribution of competing ions around DNA in solution.

The competition of monovalent and divalent cations for proximity to negatively charged DNA is of biological importance and can provide strong constraints for theoretical treatments of polyelectrolytes. Resonant x-ray scattering experiments have allowed us to monitor the number and distribution of each cation in a mixed ion cloud around DNA. These measurements provide experimental evidence to support a general theoretical prediction: the normalized distribution of each ion around polyelectrolytes remains constant when ions are mixed at different ratios. In addition, the amplitudes of the scattering signals throughout the competition provide a measurement of the surface concentration parameter that predicts the competition behavior of these cations. The data suggest that ion size needs to be taken into account in applying Poisson-Boltzmann treatments to polyelectrolytes such as DNA.

Cations↗
PubMed2004

Effects of peripheral benzodiazepine receptor ligands on proliferation and differentiation of human mesenchymal stem cells.

The peripheral benzodiazepine receptor (PBR) has been known to have many functions such as a role in cell proliferation, cell differentiation, steroidogenesis, calcium flow, cellular respiration, cellular immunity, malignancy, and apoptosis. However, the presence of PBR has not been examined in mesenchymal stem cells. In this study, we demonstrated the expression of PBR in human bone marrow stromal cells (hBMSCs) and human adipose stromal cells (hATSCs) by RT-PCR and immunocytochemistry. To determine the roles of PBR in cellular functions of human mesenchymal stem cells (hMSCs), effects of diazepam, PK11195, and Ro5-4864 were examined. Adipose differentiation of hMSCs was decreased by high concentration of PBR ligands (50 microM), whereas it was increased by low concentrations of PBR ligands (<10 microM). PBR ligands showed a biphasic effect on glycerol-3-phosphate dehydrogenase (GPDH) activity. High concentration of PBR ligands (from 25 to 75 microM) inhibited proliferation of hMSCs. However, clonazepam, which does not have an affinity to PBR, did not affect adipose differentiation and proliferation of hMSCs. The PBR ligands did not induce cell death in hMSCs. PK11195 (50 microM) and Ro5-5864 (50 microM) induced cell cycle arrest in the G(2)/M phase. These results indicate that PBR ligands play roles in adipose differentiation and proliferation of hMSCs.

Anti-Anxiety Agents↗
PubMed2004

Additive effect of the mutations in the beta3-adrenoceptor gene and UCP3 gene promoter on body fat distribution and glycemic control after weight reduction in overweight subjects with CAD or metabolic syndrome.

OBJECTIVE: To analyze the effects of the mutations in the beta3-adrenoceptor (beta3-AR) gene and/or uncoupling protein3 (UCP3) gene promoter on body fat distribution and glycemic control after mild weight reduction in overweight-obese subjects with coronary artery disease (CAD) or metabolic syndrome. DESIGN: Clinical intervention study of the -300 kcal/day mild weight reduction program for 12 weeks. SUBJECTS: A total of 224 overweight-obese subjects with CAD or metabolic disorder, subdivided into the following four categories: (1) wild type (TT-CC, n=73); (2) only UCP3 promoter variant (TT-CT/TT, n=90); (3) only beta3-AR variant (TA/AA-CC, n=29); (4) both variants (TA/AA-CT/TT, n=32). MEASUREMENT: Body mass index (BMI), blood pressure, calorie intakes, body fat distribution, serum glucose, insulin, free fatty acids, C-peptide and lipids before and after weight reduction. RESULTS: After 12 weeks, all subjects lost approximately 5% of their initial body weight. Despite similar weight reduction, the highest decreases in abdominal adipose tissue at both L1 and L4 levels were observed in the 'wild-type' group (P<0.001) and the second highest in 'only UPC3 promoter variant' group (P<0.001). On the other hand, both variant-carriers had the smallest reduction only in visceral fat area at the L4 level. All subjects except both variant-carriers showed significant reductions in the fasting levels of glucose and FFA. The response areas of glucose (P<0.01) and insulin (P<0.05) were reduced largest in the 'wild-type' group and second largest in the 'UCP3 promoter variant' group. CONCLUSION: All the four groups showed similar weight reduction after -300 kcal/d for 12 weeks. However, the beneficial effects on body fat distribution and glycemic control were greatest in the 'wild-type' group and smallest in 'both variants' group. In addition, these effects were less beneficial in carriers with beta3-AR gene variant than with UCP3 gene promoter variant.

Adipose Tissue↗
PubMed2003

Impact of genetic polymorphisms on heart failure prognosis.

Recent progress in genomic applications have led to a better understanding of the relationship between genetic background and cardiovascular diseases such as heart failure. The broad variability in heart failure patient outcome is in part secondary to modifier genes, i.e. genes that are not involved in the genesis of a disease but modify the severity of the phenotypic expression once the disease has developed. The strategy most commonly used to identify modifier genes is based on association studies between the severity of the phenotype and the sequence variation(s) of selected candidate gene(s). Using this strategy, several polymorphisms of the beta 1 and beta 2-adrenergic receptors genes and the angiotensin converting enzyme gene have been correlated to the prognosis of patients with heart failure. Recently, we have applied an experimental strategy, known as genome mapping, for the identification of heart failure modifier genes. Genome mapping has previously been used with success to identify the genes involved in the development of both monogenic and multifactorial diseases. We have shown that the prognosis of heart failure mice, induced through calsequestrin overexpression, is linked to two Quantitative Trait Loci localized on chromosomes 2 and 3. Using both strategies (candidate gene and genome mapping) should allow us to identify a number of modifier genes that may provide a more rational approach to identify patients with the worst prognosis and to predict their response to therapy.

AMP Deaminase↗
PubMed2003

Modifier genes and heart failure.

Recent progress in genomic applications have led to a better understanding of the relationship between genetic background and cardiovascular diseases such as heart failure. A considerable component of the variability in heart failure outcome is due to modifier genes, i.e. genes that are not involve in the genesis of a disease but modify the severity of the phenotypic expression once the disease has developed. The strategy most commonly used to identify modifier genes is based on association studies between the severity of the phenotype of the disease (morbidity and/or mortality) and the sequence variation(s) of selected candidate gene(s). This strategy has showed that several polymorphisms of the beta1 and beta2 adrenergic receptors genes and the angiotensin converting enzyme gene are correlated to the prognosis of patients with heart failure. Recently, we have applied an experimental strategy, known as genome mapping, for the identification of heart failure modifier genes. Genome mapping has previously been used with success to identify the genes involved in the development of both monogenic and multifactorial diseases. We have showed that the prognosis of heart failure mice, induced through overexpressing calsequestrin, is linked to 2 Quantitative Trait Loci (QTL) localized on chromosome 2 and 3. Using both strategies (candidate gene and genome mapping) should allow us to identify a number of modifier genes that may provide a more rational approach to identify patients at risk for disease and response to therapy.

Calsequestrin↗
PubMed2001

Localization of three types of the inositol 1,4,5-trisphosphate receptor/Ca(2+) channel in the secretory granules and coupling with the Ca(2+) storage proteins chromogranins A and B.

Although the role of secretory granules as the inositol 1,4,5-trisphosphate (IP(3))-sensitive intracellular Ca(2+) store and the presence of the IP(3) receptor (IP(3)R)/Ca(2+) channel on the secretory granule membrane have been established, the identity of the IP(3)R types present in the secretory granules is not known. We have therefore investigated the presence of different types of IP(3)R in the secretory granules of bovine adrenal medullary chromaffin cells using immunogold electron microscopy and found the existence of all three types of IP(3)R in the secretory granules. To determine whether these IP(3)Rs interact with CGA and CGB, each IP(3)R isoform was co-transfected with CGA or CGB into NIH3T3 or COS-7 cells, and the expressed IP(3)R isoform and CGA or CGB were co-immunoprecipitated. From these studies it was shown that all three types of IP(3)R form complexes with CGA and CGB in the cells. To further confirm whether the IP(3)R isoforms and CGA and CGB form a complex in the secretory granules the potential interaction between all three isoforms of IP(3)R and CGA and CGB was tested by co-immunoprecipitation experiments of the mixture of secretory granule lysates and the granule membrane proteins. The three isoforms of IP(3)R were shown to form complexes with CGA and CGB, indicating the complex formation between the three isoforms of IP(3)R and CGA and CGB in the secretory granules. Moreover, the pH-dependent Ca(2+) binding property of CGB was also studied using purified recombinant CGB, and it was shown that CGB bound 93 mol of Ca(2+)/mol with a dissociation constant (K(d)) of 1.5 mm at pH 5.5 but virtually no Ca(2+) at pH 7.5. The high capacity, low affinity Ca(2+)-binding property of CGB at pH 5.5 is comparable with that of CGA and is in line with its role as a Ca(2+) storage protein in the secretory granules.

3T3 Cells↗
PubMed2001

Potential role of leptin in angiogenesis: leptin induces endothelial cell proliferation and expression of matrix metalloproteinases in vivo and in vitro.

Leptin, the product of ob gene, is an endocrine hormone that regulates adipose tissue mass. Recently, leptin has been found to generate a growth signal involving a tyrosine kinase-dependent intracellular pathway and promote angiogenic processes via activation of leptin receptor (Ob-R) in endothelial cells. However, it is not clear how leptin functions to promote multi-step processes involved in the neovascularization at the atherosclerotic plaque. We have examined the expression of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) and Ob-R in human atherosclerotic lesions, leptin-mediated angiogenesis in vivo and in vitro. Immunohistochemical analysis of human atherosclerotic aorta revealed an increased expression of Ob-R in the intima of neorevascularized regions and of both MMPs and TIMPs predominantly in the endothelial lining of intimal neovessels and macrophages/foam cells. In the rat corneal angiogenesis assay, leptin elicited a comparable sensitivity of angiogenic activity to those of vascular endothelial growth factor (VEGF). The immunohistological analysis of the leptin-treated rat cornea showed definitive rises in Ob-R, MMPs and TIMPs expression as well as those of VEGF receptor (VEGFR-1). Leptin (10-40 ng/ml) induced proliferation of the human umbilical vein endothelial cells (HUVECs) and elevation of MMP-2, MMP-9, TIMP-1, and TIMP-2 expression in a dose-dependent manner. Leptin also induced increases of MMP-2, MMP-9, TIMP-1, and Up-regulated the human coronary artery smooth muscle cells (HCASMCs). These findings suggest that leptin, a hormone with pluralistic properties including a mitogenic activity on vascular endothelial cells, plays a role in matrix remodeling by regulating the expression of MMPs and TIMPs. Taken together, our findings further provide evidences for leptin's role as an angiogenesis inducer in the normal organ (rat cornea) and in aberrant vasculature under duress like atherosclerosis.

Animals↗
PubMed2001

A novel recombinant basic fibroblast growth factor and its secretion.

Basic fibroblast growth factor (FGF-2) is a pleiotropic mitogen which plays an important role in cell growth, differentiation, migration, and survival in different cells and organ systems. Recently, several clinical applications for FGF-2 gene transfer are being evaluated in wound healing and collateral artery development to relieve myocardial and peripheral ischemia due to the ability of FGF-2 to regulate the growth and function of vascular cells. However, FGF-2 lacks a classical hydrophobic secretion signal peptide, the FGF-2 chimeras containing various signal sequences have been explored. In this study, a novel recombinant 4sFGF-2 was constructed by replacing nine residues from the amino-terminus of native FGF-2 (Met1 to Leu9) with eight amino acid residues of signal peptide of FGF-4 (Met1 to Ala8) to better increase the secretion level of FGF-2. When the recombinant FGF-2 gene, cloned into the expression vector with CMV promoter, was expressed in COS-7 cells, the recombinant 4sFGF-2 was highly secreted into the media. The secreted 4sFGF-2 showed the same biological activity as the native FGF-2 in the dose-response effects on DNA synthesis and cell growth of rat aortic smooth muscle cells (RASMCs) and NIH3T3 cells. The 4sFGF-2 also was able to activate MAPK as wild FGF-2 in RASMCs. These results indicate that a novel recombinant 4sFGF-2 may be useful as clinical applicability of angiogenic growth factor gene transfer.

3T3 Cells↗
PubMed2001

Expression and tyrosine phosphorylation of E-cadherin, beta- and gamma-catenin, and epidermal growth factor receptor in cervical cancer cells.

OBJECTIVES: The cadherin/catenin adhesion complex is fundamentally involved in epithelial cancer invasion and metastasis. Much evidence suggesting that epidermal growth factor (EGF) induced the scattering and invasion of cancer cells, probably by affecting E-cadherin function, has been reported. The present study aimed to confirm the hypothesis that EGF/epidermal growth factor receptor (EGFR) was related with the E-cadherin adhesion system in cervical cancer cells and that EGF might induce tyrosine phosphorylation of beta- and gamma-catenin. METHODS: Cervical cancer cells were treated for different time durations with 30 ng/ml of EGF. Alteration of the cell morphology was examined by light microscopy and the expression of E-cadherin, beta-catenin, gamma-catenin, EGFR, and activated EGFR was assayed using Western blotting. Tyrosine phosphorylation of beta- and gamma-catenin was also examined using immunoprecipitation. RESULTS: E-cadherin and EGFR were expressed in CaSki, HT-3, and ME-180 cell lines, which showed epithelial contact growth. The expression of E-cadherin and beta- and gamma-catenin did not change after treatment with EGF. The expression of EGFR decreased and activated EGFR expression increased in 30 min and then decreased subsequently. The simultaneous expression of activated EGFR and tyrosine phosphorylation of beta- and gamma-catenin was found. CONCLUSIONS: EGF-induced scattering of the E-cadherin-positive cervical cancer cells might be the result of tyrosine phosphorylation of the beta- and gamma-catenin. Phosphorylation of the beta- and gamma-catenin may hamper the adhesive function of the E-cadherin-catenin complex.

Blotting, Western↗
PubMed2001

Effects of heme oxygenase system on the cyclooxygenase in the primary cultured hypothalamic cells.

Endogenous carbon monoxide (CO) shares with nitric oxide (NO) a role as a putative neural messenger in the brain. Both gases are believed to modulate CNS function via an increase in cytoplasmic cGMP concentrations secondary to the activation of soluble guanylate cyclase (sGC). Recently CO and NO were proposed as a possible mediator of febrile response in hypothalamus. NO has been reported to activate both the constitutive and inducible isoform of the cyclooxygenase (COX). Thus, we investigated whether CO arising from heme catabolism by heme oxygenase (HO) is involved in the febrile response via the activation of COX in the hypothalamus. PGE2 which is a final mediator of febrile response released from primary cultured hypothalamic cells was taken as a marker of COX activity. PGE2 concentration was measured with EIA kits. Exogenous CO (CO-saturated medium) and hemin (a substrate and potent inducer of HO) evoked an increase in PGE2 release from hypothalamic cells, and these effects were blocked by methylene blue (an inhibitor of sGC). And membrane permeable cGMP analogue, dibutyryl-cGMP elicited significant increases in PGE2 release. These results suggest that there may be a functional link between HO and COX enzymatic activities. The gaseous product of hemin through the HO pathway, CO, might play a role through the modulation of the COX activity in the hypothalamus.

Animals↗
PubMed2001

The apolipoprotein(a) size, pentanucleotide repeat, C/T(+93) polymorphisms of apolipoprotein(a) gene, serum lipoprotein(a) concentrations and their relationship in a Korean population.

BACKGROUND: In addition to apolipoprotein(a) [apo(a)] kringle 4 variable number of tandem repeat (K4-VNTR), pentanucleotide repeat polymorphism (PNRP) and C/T(+93) polymorphism [C/T(+93)] of apo(a) gene have been suggested to be related to lipoprotein(a) [Lp(a)] concentration. We studied the distribution of these genetic polymorphisms and their relationship with Lp(a) concentrations in a Korean population. METHODS: One hundred thirty-two Korean adults were examined. Lp(a) was measured with enzyme-linked immunosorbent assay (ELISA). Apo(a) K4-VNTR was measured by high-resolution SDS-agarose gel separation and ECL Western blotting method. PNRP was measured after DNA amplification. The C/T(+93) ratio was measured by a amplification refractory mutation system. RESULTS: Lp(a) was inversely correlated with K4-VNTR (r=0.732, p<0.0001), but was associated neither with any PNRP haplotype nor with C/T(+93) by multiple regression analysis, although we found a significant decrease of Lp(a) in PNRP 9/9 individuals (p<0.01). There was a strong linkage disequilibrium between 9 haplotypes of PNRP and the T haplotype of C/T(+93). CONCLUSIONS: Inverse relationship between serum Lp(a) and K4 number of apo(a) was confirmed in normal Korean adults. PNRP 9/9 genotype appeared to have a reducing effect on Lp(a), but neither 9 haplotype heterozygotes of PNRP nor the T haplotype C/T(+93) affected Lp(a) concentrations in Koreans.

Apolipoproteins A↗
PubMed2001

A novel pH-sensitive membrane from chitosan--TEOS IPN; preparation and its drug permeation characteristics.

A novel organic-inorganic composite membrane was prepared, using tetra ethyl ortho silicate (TEOS) as an inorganic material and chitosan as an organic compound. Equilibrium and oscillatory swelling studies were conducted to investigate swelling behaviors of the membrane according to the pH of the swelling medium. Drug permeation experiments were also performed in phosphate buffer solution of the pH of 2.5 and 7.5, respectively. Lidocaine HCl, sodium salicylate and 4-acetamidophenol were selected as model drugs to examine the effect of ionic property of drug on the permeation behavior. The effects of membrane composition and the external pH on the swelling and the drug permeation behavior of IPN membrane could be summarized as follows; chitosan incorporated into TEOS IPN swelled at pH 2.5 while shrunk at pH 7.5. This swelling behavior was completely reversible and the membrane responded rapidly to the change in environmental pH condition. According to swelling behavior, an increase in pH from 2.5 to 7.5 yielded an increase in the rate of drug permeation because of the shrinking of the incorporated chitosan in TEOS IPN, while decrease in pH resulted in low permeation rate. The optimal TEOS-chitosan ratio for maximum pH-sensitivity existed and drug permeation was influenced not only with the external pH but also with the ionic interactions between the drug and membrane.

Chitin↗
PubMed2001

Changes in cellular motility and cytoskeletal actin in fibroblasts from patients with chronic venous insufficiency and in neonatal fibroblasts in the presence of chronic wound fluid.

PURPOSE: Fibroblasts (fb) play an important role in wound healing involving motility, contraction, fibrosis, and expression of the cytoskeletal protein alpha-smooth muscle actin (alpha-sma). Patients with chronic venous insufficiency (CVI) are known to have dermal changes and impaired venous ulcer healing. To investigate whether these dermal-fb have an altered ability to migrate and whether chronic wound fluid from venous ulcers alters neonatal fb motility, we examined cell migration and alpha-sma. METHODS: Fibroblasts were cultured from the margin of venous ulcers (du-fb, n = 4, CEAP 6), from patients with venous reflux without ulcer (dr-fb, n = 5, CEAP 2), and from the ipsilateral thigh of the same patients with (pu-fb) and without (pr-fb) ulcer, respectively. The abbreviations used are p and d, which represent proximal and distal, respectively; u and r represent ulcer and reflux, respectively. Neonatal foreskin fibroblasts (nf-fb) were exposed to chronic venous ulcer wound fluid (CVUWF, 300 microg protein/mL, n = 3) or bovine serum albumin (BSA, control). Fibroblast motility was determined by means of time-lapse photo-images, and the rate (micrometer per hour) was calculated. Immunohistochemistry for alpha-sma was analyzed with confocal laser microscopy. RESULTS: The rate of motility (micrometer per hour +/- SEM) was decreased for both du-fb (11.4 +/- 0.7) and dr-fb (13.8 +/- 0.6), when compared with pu-fb (21.9 +/- 0.9) and pr-fb (24.7 +/- 1.1), respectively. The motility rate for nf-fb was lower in CVUWF (24.7 +/- 2.0) than in BSA (37.1 +/- 6.7). An elevated level of microfilament bundles of alpha-sma for both du-fb and dr-fb, compared with those of pu-fb and pr-fb, and also in nf-fb treated with CVUWF was demonstrated by means of immunohistochemistry. CONCLUSION: These data demonstrate a reduced motility in the dermal fb of patients with CVI. Patients with reflux disease without ulcer are predisposed to these changes. Furthermore, it appears that CVUWF causes changes in motility and alpha-sma expression in nf-fb as demonstrated in du-fb. These findings suggest that reduced motility and CVUWF, representing the microenvironment of venous ulcers, play a significant role in impaired wound healing.

Actins↗
PubMed2001

Optimal concentration of human epidermal growth factor (hEGF) for epithelial healing in experimental corneal alkali wounds.

PURPOSE: By using both in vivo and in vitro (organ-cultured) systems, the optimal concentrations of hEGF to enhance epithelial healing after alkali wounds were evaluated in the rabbit cornea. METHODS: Alkali-injured corneas (pi = 5.5 mm, 1 N NaOH, 60 s) were treated with 0.01, 0.1, 1.0, 10 and 100 ng/ml hEGF for the in vitro study. The healing of epithelium and endothelium was determined at 1, 2, 3, 4, and 6 days after treatment. For the in vivo experiment, the eyes were treated with 2, 5, 10, and 50 microg/ml hEGF 3 times per day. The measurement of epithelial healing rate, transmission electron microscopy and immunohistochemical observation were performed after 7 days treatment. RESULTS: In in vitro tests, hEGF enhanced the epithelial healing rates, showing a maximum enhancement at the concentration of 1.0 ng/ml, and endothelial healing was increased at 100 ng/ml. In in vivo studies, no significant difference was observed in the rates of epithelial healing between control and each hEGF-treated group. Among the tested concentrations, 5 microg/ml hEGF induced the most active proliferation of basal cells and 50 microg/ml hEGF remarkably produced a vascular ingrowth to the central wound area. The thickness of re-surfaced epithelium was increased by hEGF in a concentration-dependent manner. CONCLUSIONS: The results of the present study indicate that a low concentration of hEGF may selectively enhance epithelial healing without affecting endothelial healing. The optimal concentration of hEGF for the stimulation of epithelial healing appears to be 5 microg/ml in rabbit corneal alkali wounds.

Animals↗