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PubMed1984

Serum levels of type I and III procollagen fragments in Paget's disease of bone.

Patients with Paget's disease of bone were found to have elevated serum levels of type I procollagen carboxyterminal peptide (pColl-I-C) which correlated with other measurements of disease activity. The elevated levels of pColl-I-C decreased within hours after the injection of salmon calcitonin and within weeks after oral dichloromethylene diphosphonate treatment. The decrease in serum pColl-I-C after a single injection of salmon calcitonin was associated with a decrease in urinary hydroxyproline excretion, both of which rose toward pretreatment values within 7 h. The pColl-I-C levels remained normal for months after dichloromethylene diphosphonate therapy was discontinued. Using a RIA for the type III procollagen amino-terminal peptide (pColl-III-N), it was found that serum levels were also elevated in patients with Paget's disease. The levels of pColl-III-N also decreased after the injection of salmon calcitonin, but not to the same extent as those of pColl-I-C. After chronic therapy with dichloromethylene diphosphonate, serum levels of pColl-III-N decreased, but not into the normal range. We postulate that whereas pColl-I-C is derived from synthesis of mineralized bone collagen, pColl-III-N is derived from the loose fibrous stroma replacing marrow in areas closely associated with active Pagetic bone disease.

Antibody Specificity↗
PubMed1990

Comparative study of the changes in insulin-like growth factor-I, procollagen-III N-terminal extension peptide, bone Gla-protein, and bone mineral content in children with Turner's syndrome treated with recombinant growth hormone.

Six girls (7-13 yr old) with Turner's syndrome and short stature were treated for 1 yr with recombinant human GH (0.15 U/kg.day, sc) and had sequential determinations of serum insulin-like growth factor-I (IGF-I), osteocalcin, and procollagen-III. Bone mineral content and density of the spine and radius were measured before treatment and at 90 and 360 days. Two girls received small doses of ethinyl estradiol (0.025 micrograms/kg) in addition to GH. Height velocity increased by 144% after 3 months of treatment. IGF-I was normal (0.75 +/- 0.20 kU/L) before treatment and increased by 90% on day 1 and by 290% on day 360. Procollagen-III was low before treatment; it peaked at 53.0 +/- 14.7 micrograms/L (260% above baseline) on day 30, then decreased to the normal range. Serum osteocalcin increased more slowly to reach a plateau on day 90 of 23.7 +/- 1.2 micrograms/L (46% above baseline). Before treatment, bone mineral content of the spine was 25% lower than that of children matched for bone age. Bone mineral contents of the peripheral and axial skeleton were increased by 10% and 17%, respectively, after 1 yr of treatment, an increase commensurate with that of bone age in the four patients who did not receive estrogen. On day 90, however, although radius mineral density was already increased by 3%, the mineral density of the lumbar spine was significantly decreased by 4%. We conclude that treatment with GH increases IGF-I, collagen turnover, osteoblastic function, and height velocity in Turner's syndrome. However, there is no catch-up of bone mineral content after 1 yr of treatment, and an early effect of GH is to decrease spine mineral density.

Adolescent↗
PubMed1990

Elevated serum procollagen III aminopeptide levels in sarcoidosis.

Procollagen III aminopeptide (P-III-P), a peptide released during the conversion of type III procollagen to type III collagen, is considered a potential marker of fibroblast activity in a variety of pulmonary and extrapulmonary diseases. The aim of the present article was to investigate the levels of P-III-P in serum samples (sP-III-P) from a large number of sarcoid patients, in particular looking at its relationship with other markers of disease activity and its presumed role as a marker of pulmonary fibrosis. sP-III-P has been radioimmunoassayed in an overall series of 57 patients and the levels were higher (19.18 +/- 9.17 ng/ml) than in 25 age- and sex-matched controls (11.32 +/- 2.15 ng/ml; p less than 0.001). The elevation was neither sex-related nor related to obvious liver sarcoid localization. Although sP-III-P levels were slightly higher in patients with stage II, there was no significant difference in patients with stage I or III. We found a positive relationship with serum angiotensin-converting enzyme (S-ACE) levels (p less than 0.04), but not with other markers of disease activity (67Ga uptake, bronchoalveolar lavage [BAL] lymphocyte percent, vital capacity, and lung diffusing capacity). The relationship with S-ACE was confirmed in a longitudinal follow-up study, where sP-III-P strictly paralleled the S-ACE behavior. Finally, the initial sP-III-P levels did not predict cases either with disease relapse or resistance to corticosteroid treatment. We conclude that, in our study, sP-III-P levels failed to characterize sarcoid patients with radiologic fibrotic pattern (stage III), and, in addition, were unable to predict which patients would have a poor prognosis. Rather, they reflect a metabolic activity of sarcoid granuloma cells. Thus, the usefulness of sP-III-P in the treatment of patients with sarcoid may be considered similar to that of S-ACE.

Adult↗
PubMed1998

Carboxyl-terminal parathyroid hormone fragments stimulate type-1 procollagen and insulin-like growth factor-binding protein-5 mRNA expression in osteoblastic UMR-106 cells.

The effects of carboxyl-terminal (C-) PTH fragments, (35-84), (53-84) and (69-84), on the proliferation and function of osteoblastic UMR-106 cells were compared with those of amino-terminal (N-) (1-34) and intact (I-) (1-84) PTH. I-PTH as well as N-PTH at 10(-8)M significantly inhibited [3H] thymidine incorporation and stimulated alkaline phosphatase activity in UMR-106 cells. No C-PTH fragments affected them. In contrast, the expression of type-1 procollagen mRNA in these cells was stimulated by all C-PTH fragments, inhibited by N-PTH and not affected by I-PTH. All C-PTH fragments except (69-84) as well as N-PTH and I-PTH stimulated IGFBP-5 mRNA expression. The present study suggests that the C-portion of the PTH molecule exercises biological activities in mRNA expression of type-1 procollagen as well as IGFBP-5 in osteoblasts, and that it might be involved in the anabolic action of PTH on bone in vivo.

Cell Line↗
PubMed1999

Plasma insulin-like growth factor-1, type 1 procollagen, and serum tumor necrosis factor alpha in children recovering from Trichuris dysentery syndrome.

OBJECTIVES: To explore: 1) the relationship between plasma insulin-like growth factor-1 (IGF-1) and other markers of growth; and 2) the effect of serum concentrations of tumor necrosis factor alpha (TNF) on growth variables in children (2-10 years) stunted by Trichuris dysentery syndrome (TDS), recovering cases, and their matched controls. METHOD: Fourteen patients with TDS were admitted to the Tropical Metabolism Research Unit, treated with albendazole and iron, and then followed with matched controls (n = 28) for 1 year. Anthropometric and biochemical measurements were done on admission and then every 3 months for the year. Plasma IGF-1, the carboxyterminal propeptide of type 1 procollagen, serum TNF, total serum protein, serum albumin, and complete blood count were determined. RESULTS: Low admission plasma levels of IGF-1 in TDS cases were accompanied by high serum levels of TNF, and total serum protein, normal serum albumin, low hemoglobin, reduced collagen synthesis (low plasma carboxyterminal propeptide of type 1 procollagen), and growth failure. These variables improved significantly after treatment. Plasma levels of IGF-1 were significantly related to the Z-scores for height-for-age (r = 0.60, 0.73, 0.68) and weight-for-age (r = 0.69, 0.80, 0.69) of cases and controls, height-for-age (r = 0.51, 0.52, 0.54) and weight-for-age (r = 0.51, 0.52, 0.54) at each measurement throughout the year. Serum levels of TNF were not related to any of the growth variables. CONCLUSION: These findings may contribute to the understanding of growth failure in children affected by other forms of chronic inflammatory bowel disease.

Animals↗
PubMed2000

Effect of a ceramic and a non-ceramic hydroxyapatite on cell growth and procollagen synthesis of cultured human gingival fibroblasts.

BACKGROUND: Ceramic hydroxyapatites and non-ceramic hydroxyapatites have been used extensively as alloplastic materials for bone reconstruction. However, different forms of hydroxyapatite induce different types of tissue response. METHODS: Human gingival fibroblasts (FMM1 cells) were used to analyze ceramic and non-ceramic hydroxyapatite biocompatibility. The cells were grown on surfaces covered either by collagen (control group), collagen plus ceramic hydroxyapatite, or collagen plus non-ceramic hydroxyapatite. Scanning electron microscopy, growth and cell viability curves, and procollagen immunoprecipitation were obtained. For the growth and viability curves, 10(4) cells were seeded on 60 mm dishes. Cells from each group were counted, in triplicate, at 1, 3, 4, 5, and 6 days after seeding using the Trypan blue dye exclusion assay. RESULTS: The cells grew in close contact with both types of hydroxyapatite particles. No differences were found in the amount of procollagen synthesis among any experimental group. The cultures treated with ceramic hydroxyapatite had a growth delay for the first 5 days. There was no difference in cell viability between the control group and the non-ceramic hydroxyapatite group. However, cultures treated with ceramic hydroxyapatite showed significantly lower viability percentages than the other groups. CONCLUSIONS: Hydroxyapatite supports cell growth and fibroblast metabolism including collagen production, and hence is biocompatible. Cell viability and structural studies showed that non-ceramic hydroxyapatite has relevant physical and biological properties as an implant material.

Algorithms↗
PubMed1999

Increase in expression of Hsp47 and collagen in hereditary gingival fibromatosis is modulated by stress and terminal procollagen N-propeptides.

HGF is a rare oral condition characterized by a slow, progressive enlargement of the gingiva, involving both the maxilla and mandible. HGF provides a model for the study of regulatory features of conditions characterized by connective tissue hyperplasia. In this study, the culture characteristics of gingival fibroblasts derived from patients of the same family with HGF (n = 4) were similar with regard to cell cycle analysis. Flow cytometric DNA content analysis revealed uniform DNA diploidy for fibroblasts cultured from NG and HGF. NG cells showed a low S-phase fraction (19.8%) and G2/M fraction (5.8%) and a relatively high G1 phase fraction (74%). In contrast, HGF cells from all members of the tested kindred, exhibited diploid cells with a higher S-phase (40.9%) and G2/M (10.1%) fraction and a relatively low G1 phase fraction (40.9%). Furthermore, we demonstrated that the expression and production of Hsp47 parallels the increased levels of collagen secretion observed in HGF. In addition, we show that Hsp47 and collagen are coordinately regulated following stress via a feedback mechanism mediated by N-terminal procollagen propeptides. Utilizing confocal microscopy and antibodies directed against GST-fusion proteins encompassing the pro alpha1(I) N-propeptide globular domain (NP1) (residues 23-108), it was apparent that this regulatory mechanism does not involve significant interaction with Hsp47's chaperoning of procollagen.

Cells, Cultured↗
PubMed2003

Elevated serum values of procollagen III peptide (PIIIP) in patients with ulcerative colitis who will develop pseudopolyps.

AIM: To assess the impact of procollagen III peptide as a marker of collagenesis in the development of pseudopolyps in patients with ulcerative colitis. METHODS: Development of pseudopolyps was monitored in 25 patients with ulcerative colitis classified according to Powell-Tuck index as mild (n=12) or moderate (n=13) form of disease. Patients with a mild form of disease were treated with oral mesalazine medication (2-4 g/day) and local mesalazine preparation (suppository). Patients with a moderate form of disease received oral mesalazine medication (2-4 g/day), local mesalazine preparation (suppository) and local methylprednisolone at an initial dose of 60 mg/day, followed by dose tapering. How many significant variables (previously determined by analysis of variance) were elevated in the groups with and without pseudopolyp developement was observed. ROC analysis for calculation of new index was made. RESULTS: Serum values of procollagen III peptide (PIIIP), C-reactive protein (CRP) and C4 complement component (C4) were statistically significantly lower in the group of patients free from pseudopolyp development than those who developed one or more pseudopolyps (0.45+/-0.12 vs 1.42+/-0.70, P<0.0027; 7.6+/-4.7 vs 17.8+/-9.17, P<0.035; and 0.46+/-0.11 vs 0.34+/-0.16, P<0.068, respectively) at endoscopic conrtrols with patohistologically samples during 13 months. There were no statistically significant differences in the values of C3, ceruloplasmin and IgM between the two groups (P>0.05). Discrimination function analysis yielded highest standardized cannon coefficients for PIIIP (0.876), CRP (0.104), C3 (-0.534) and C4 (0.184) (P<0.036). The elevation in two of three laboratory variables (PIIIP, CRP and C4) reached sensitivity of 93 % and specificity of 90 % in the development of pseudopolyps. CONCLUSION: It is proposed that an increase in two of the three laboratory parameters (PIIIP, CRP and C4) could improve the accuracy of prediction of the development of pseudopolyps. When using PIIIP, CRP and C4 on decision making, the positive predictive value and accuracy were 90 % and 92 %, respectively.

Adult↗
PubMed2002

Imbalance in the expression of CXC chemokines correlates with bronchoalveolar lavage fluid angiogenic activity and procollagen levels in acute respiratory distress syndrome.

Diffuse alveolar damage is the histopathological hallmark of acute respiratory distress syndrome (ARDS) and is a stereotypic response to a variety of etiologies. Moreover, a significant proportion of ARDS survivors have residual pulmonary fibrosis and compromised pulmonary function. This suggests that the pathogenesis of diffuse alveolar damage that ultimately leads to the chronic fibrosis of ARDS has features of dysregulated repair exemplified by exaggerated intra-alveolar angiogenesis and fibrogenesis (i.e., fibroproliferation and deposition of extracellular matrix), leading to progressive alveolar fibrosis and impaired lung function. We obtained bronchoalveolar lavage fluid (BALF) from patients with ARDS or ventilated control patients and assessed CXC chemokine levels by ELISA. We found an imbalance in the expression of ELR(+) as compared with ELR(-) CXC chemokines from BALF of patients with ARDS as compared with controls. This imbalance correlated with angiogenic activity as assessed by the corneal micropocket assay. Furthermore, these levels correlated with both procollagen I and procollagen III levels in BALF. In contrast, while BALF levels of vascular endothelial growth factor were elevated, vascular endothelial growth factor did not appear to be significantly contributing to the angiogenic activity. These findings suggest that CXC chemokines have an important role in the fibroproliferative phase of ARDS via the regulation of angiogenesis.

Amino Acid Motifs↗
PubMed1999

[Changes in TGF-beta 1 and type I, III procollagen gene expression in keloid and hypertrophic scar].

OBJECTIVE: The expression of mRNA for TGF-beta 1, type I, III procollagen in keloid and hypertrophic scar was investigated in order to elucidate the pathogenesis of and the difference between keloid and hypertrophic scar. METHOD: Dot-blot hybridization analysis was used to examine the type I, III procollagen and the expression levels of steady-state mRNA. In situ hybridization allowed direct assessment of the distribution of TGF-beta 1 mRNA in the tissue. RESULTS: 1. Our study indicated that the expression level of mRNA for TGF-beta 1 significantly increased in keloid and hypertrophic scar compared with normal scar and normal skin. 2. In keloid tissues, type I precollagen mRNA expression was selectively increased. However, in hypertrophic scar, type I and III collagen mRNAs expressions were simultaneously increased. CONCLUSION: TGF-beta 1 plays an important role in the pathogenesis of keloid and hypertrophic scarring. It implicates that distinct molecular mechanisms are operative in the development of keloid and hypertrophic scarring.

Cicatrix, Hypertrophic↗
PubMed1992

[Expression of type I and type III procollagen genes in human scirrhous carcinoma of breast by in situ hybridization].

Scirrhous carcinoma is characterized by remarkable amount of collagen fibrils, mainly Type I and Type III collagens. The origin of the collagens is still under debate. cDNA fragments of Type I and Type III procollagens were subcloned into Gemini pGEM vectors to synthesize the 35S-labeled cRNA probes. By in situ hybridization, we have found the fibroblasts surrounding the tumor cells and cords contained abundant Type I and Type III procollagen mRNAs which decreased with the distance of fibroblasts from the tumor cells. In all freshly prepared tissues, the tumor cells also contained significant pro alpha 1(I) and pro alpha 1(III) mRNAs, but no or little pro alpha 2(I) mRNA. The results indicated that Type I and Type III collagens in human scirrhous carcinoma of breast are mainly produced by fibroblasts. Tumor cells also participate in the disposition of collagen fibrils, probably Type I trimer and Type III collagens in accordance with what was observed in biochemical analysis and cell culture studies.

Adenocarcinoma, Scirrhous↗
PubMed1992

Novel amino-terminal propeptide configuration in a fibrillar procollagen undergoing alternative splicing.

We isolated overlapping cDNAs from embryonic libraries of the sea urchin Strongylocentrotus purpuratus coding for a fibrillar procollagen (2 alpha chain) with a predicted molecular mass of about 320 kDa. The deduced primary structure of the echinoid chain consists of a 265-amino acid carboxyl-propeptide, a triple helical domain made of 337 uninterrupted Gly-X-Y repeats, and an unusually long amino-propeptide. Aside from a 10-cysteine globular region, a collagenous sequence, and a nonhelical segment, this protein domain includes a novel 4-cysteine motif repeated several times. Interestingly, preliminary evidence indicates that different combinations of the 4-cysteine repeats are encoded by alternatively spliced transcripts. Irrespective of this, the sea urchin 2 alpha procollagen chain represents the longest fibrillar molecule identified to date by cDNA cloning experiments in both vertebrate and invertebrate organisms.

Amino Acid Sequence↗
PubMed1992

[Serum aminoterminal procollagen type-III peptide in the diagnosis of chronic hepatopathies].

BACKGROUND: The aims of the present study were to 1) compare the serum levels of the aminoterminal peptide of procollagen type III (PIIIP) in patients with different chronic liver diseases, 2) correlate their concentrations with histologic features in liver biopsy and 3) evaluate their use in the diagnosis of liver diseases and in recognition of fibrosis. METHODS: With these aims PIIIP was determined in 57 patients with different chronic liver diseases and in 50 healthy donors. RESULTS: PIIIP was significantly elevated in patients with chronic active hepatitis (18.3 +/- 5.5 ng/ml; p less than 0.01) and with liver cirrhosis (27.8 +/- 11.7 ng/ml; p less than 0.001). The serum levels of this peptide related significantly with the severity of liver disease (p less than 0.001) in addition to the degree of morphometric liver fibrosis (Rs: 0.736; p less than 0.001) and with the degree of histologic activity (Rs: 0.78; p less than 0.001). The correlation between PIIIP and fibrosis was due to the relation between the same and inflammation. The levels of this peptide which were higher than 15 ng/ml were a sensitive test for the diagnosis of active liver disease (0.80) and cirrhosis (0.87) permitting differentiation between chronic and persistent active hepatitis. The differentiation between chronic active hepatitis and cirrhosis was only possible when 24 ng/ml were taken as a discriminative level. CONCLUSIONS: The comparison of serum levels of the aminoterminal peptide of procollagen type III (PIIIP) in patients with different chronic liver diseases can predict moderate or high degrees of inflammatory activity when PIIIP are higher than 15 ng/ml. This test is of use for evaluating chronic hepatopathies although the levels reflect the activity of inflammation better than the degree of hepatic fibrosis.

Adult↗
PubMed2005

[Angiotensin II and aldosterone stimulate alpha1-(I) procollagen mRNA expression in hepatic stellate cells via activation of ERK1/2 and AP-1].

OBJECTIVE: To investigate the signal transduction mechanism underlying the effects of angiotensin II (Ang II) and aldosterone (Aldo) on the signal passageway of active protein-1 (AP-1). METHODS: In vitro, Hepatic stellate cells (HSCs) of the line HSC-T6 were cultured and treated with Ang II or Aldo, the principal effector molecules of the renin-angiotensin-aldosterone system (RAAS) for 10, 30, 60, 120, and 180 minutes respectively. The protein expression of phospho-P42/44 was detected by Western blotting. In addition, HSC-T6 cells were preincubated for 60 min with U0126, an inhibitor of MAPK/ERK kinase, irbesartan, an AT-1 receptor blocker, N-acetylcysteine (NAC), antioxidant, angiotensin converting enzyme inhibitor (ACEI), or tumor necrosis factor alpha (TNFalpha) prior to exposure to Ang II or Aldo. Then the protein expression of phospho-P42/44 was measured by Western blotting. The DNA biding activity of AP-1 was analyzed by electrophoretic gel mobility shift assay (EMSA). By means of RT-PCR, the mRNA expression of alpha1 (I) procollagen was detected. RESULTS: The levels of phopho-ERK1/2 protein increased after the treatment of Ang II and Aldo at all time points and both peaked 10 minutes after (both P < 0.01). The levels of phopho-ERK1/2 protein of the irbesartan + Ang II and U0126 + Ang II groups were significantly lower than that of the Ang II group (both P < 0.01). The level of phopho-ERK1/2 protein of the Ang II group was lower than that of the TNFalpha group, however, was especially significantly lower than that of the Ang II + TNFalpha group (P < 0.01). The level of phopho-ERK1/2 protein of the U0126 + Aldo group was significantly lower than that of the Aldo group (P < 0.01). The phopho-ERK1/2 protein level of the NAC + Aldo group was not significantly different from that of the Aldo group (P > 0.05). The phopho-ERK1/2 protein level of the Aldo group was lower than that of the TNFalpha group, however, was especially significantly lower than that of the Aldo + TNFalpha group (P < 0.01). The AP-1 DNA binding protein increased after the treatment of Ang II and peaked 30 min after. U0126, irbesartan, and NAC, as well as ACEUI, significantly inhibited the increased AP-1 DNA binding activity induced by Ang II. The AP-1 DNA binding protein increased after the treatment of Aldo and peaked twice, 30 min and 240 min after. U0126 and NAC significantly and NAC partly inhibited the increased AP-1 DNA binding activity induced by Aldo. CONCLUSION: Stimulation of HSC by Ang II and Aldo results in activation of AP-1 via ERK1/2 pathway leading to up-regulation of AP-1 target gene alpha1 (I) procollagen mRNA expression.

Aldosterone↗
PubMedDate not supplied

[Procollagen type III peptides in chronic viral hepatitis].

Blood serum concentration of procollagen type III peptides was assayed in 37 patients with chronic active hepatitis, 14 patients with persisting chronic hepatitis, and 11 normal subjects. Mean concentration of these peptides was significantly higher in patients with chronic active hepatitis than in those with persisting chronic hepatitis (25.6 +/- 11.5 ng/mL vs. 14.0 +/- 4.5 ng/mL; p < 0.001), and in individuals without lesions to the liver (25.6 +/- 11.5 ng/mL vs. 12.5 +/- 2.9 ng/mL; p < 0.001). Blood serum concentration of procollagen type III peptides may be helpful in the differential diagnosis of hepatitis.

Adult↗
PubMedDate not supplied

Albumin and procollagen type I gene regulation in alcohol and viral-induced human liver disease.

Common features of chronic alcoholic liver disease are progressive hypoalbuminemia and liver fibrosis. The molecular mechanisms which account for these effects are still controversial. Therefore, in the present study we evaluated albumin and collagen gene expression in livers of alcohol abusers and patients with viral-induced liver disease. Albumin and pro-alpha 1 (I) collagen mRNA levels were determined in 30 patients who underwent diagnostic liver biopsy. Of 14 alcoholics, 7 had alcoholic hepatitis alone, while the other 7 had cirrhosis plus alcoholic hepatitis. Of 16 non-alcoholic patients with chronic viral infection, 6 had chronic active hepatitis and 10 cirrhosis plus chronic active hepatitis. Total RNA was extracted from a portion of each biopsy, hybridized with a human albumin or collagen cDNA clone and compared to 2 normal surgical specimens which served as controls. The Northern hybridization studies revealed that: despite the presence of inflammation and fibrosis, the albumin mRNA levels of alcoholics were similar to normal controls; these alcoholics had significantly higher levels of albumin mRNA than did patients with similar histological stages of disease due to viral infection; and all the categories of patients had markedly increased procollagen mRNA levels when compared to controls. Given these results it is tempting to speculate that alcohol may actually increase albumin mRNA content in man as it does in animals. Furthermore, the increased procollagen mRNA levels in fibrotic livers suggest that an increase in collagen synthesis may be a significant factor in the pathogenesis of hepatic fibrosis.

Albumins↗
PubMed1991

G to T transversion at position +5 of a splice donor site causes skipping of the preceding exon in the type III procollagen transcripts of a patient with Ehlers-Danlos syndrome type IV.

We identified a splicing mutation in a patient with Ehlers-Danlos syndrome type IV, a heritable connective tissue disorder associated with dysfunctions of type III collagen. The mutation was first localized in the patient's type III procollagen mRNA by amplifying the reverse transcribed product in several overlapping fragments using the polymerase chain reaction. Amplified products spanning exon 24-26 sequences displayed two distinct fragments, one of normal size and the other lacking the 99 base pairs of exon 25. Sequencing of amplified genomic products identified a G to T transversion at position +5 of the splice donor site of intron 25 in one of the patient's procollagen III genes. Expression of allelic minigene constructs correlated the T for G substitution with skipping of exon 25 sequences. Like previously characterized splicing mutations in other collagen genes, lowering the temperature at which the patient's fibroblasts were incubated nearly abolished exon skipping. As a part of this study, we also identified a highly polymorphic, intronic DNA sequence whose different allelic forms can be detected easily by the polymerase chain reaction technique.

Alleles↗
PubMed1991

Type I and III procollagens in CAPD: markers of peritoneal fibrosis.

The carboxyterminal propeptide of type I procollagen (PICP) and the aminoterminal propeptide of type III procollagen (PIIINP) are split products related to formation of granulation tissue. Local concentrations reflect the state of fibrosis activity. PICP and PIINP were measured in serum and dialysate from 13 CAPD patients. One patient had 5-fold higher PICP and 8-fold higher PIIINP in the dialysate than the 12 other patients receiving CAPD. One month after the samples were collected, the patient was taken off CAPD due to sclerosins peritonitis. Our observation indicates that determinations of PICP and PIIINP in the dialysate could be useful markers of peritoneal fibrosis.

Biomarkers↗