Biomedical subjects

M Selman

Publications and source records attributed to M Selman.

At least 55 records · Page 3Linked to original sources

PubMed1997

BCG specificity of an inhibitory seric factor from tuberculosis anergic patients that acts on non-adherent PPD reactive cells.

The effect of tuberculosis anergic immune sera adsorbed with BCG was studied on cocultures of adherent and non-adherent cells from PPD+ tuberculosis patient (TBP PPD+). This effect on the cocultures was quantified by lymphocyte transformation (LT) test using PPD as antigen. Only those cocultures with non-adherent cells from TBP PPD+ patients treated with anergic sera, inhibited the LT response induced by PPD, whereas sera adsorption with BCG eliminated the inhibitory effect.

Adsorption↗

PubMed1997

On the correct determination of reference values for serum antibodies against pigeon serum antigen using a group of healthy blood donors.

An enzymatic immunoassay was developed in order to evaluate the statistical distribution of IgG serum antibodies against pooled pigeon sera antigen in 102 healthy blood donors (HBD). A non-normal distribution was obtained as demonstrated by abnormal values of skewness (2.02) and kurtosis (6.50). A cut-off point (0.120) was determined from the mean plus 2 standard deviations of the optical density values obtained in the HBD group. This value was able to segregate 94% of subjects. However, when calculation of the mean less 2 SD was performed to delimit 95% of the samples, an aberrant negative value was obtained. In contrast, when the nonparametric method of percentile calculation was applied, an optical density value of 0.130 discriminated 97.5% of samples. In addition, the interval between p97.5 and p2.5 delimited 95% of samples. We conclude that when reference values and cut-off point are determined from an enzymatic immunoassay, careful analysis of the statistical distribution of reference values is necessary in order to avoid the inappropriate application of parametric procedures as demonstrated in this study for antibodies against pigeon serum antigens.

Adult↗

PubMed1996

Detection of salivary and seric IgG and IgA antipooled pigeon sera activities in patients with pigeon breeder's disease.

Pigeon breeder's disease (PBD) is an interstitial lung disease induced by exposure to pigeon antigens. Search of antipigeon antigen antibodies (APSA) in serum or bronchoalveolar lavage is generally used for auxiliary diagnostic purposes. However, APSA can be present in a number of exposed but asymptomatic individuals as well as in patients with other interstitial lung diseases who live in areas where keeping pigeons is a common domestic habit. In this study, saliva was evaluated as an alternative means to serum for APSA detection by ELISA using pooled pigeon sera as antigen. Serum and saliva samples obtained from 17 patients with PBD, 14 with idiopathic pulmonary fibrosis (IPF), 19 asymptomatic relatives (AR) exposed to pigeon antigens, and 27 clinical healthy voluntary subjects (CHVS) were tested for IgG and IgA APSA. Our results showed that both fluids obtained from PBD patients exhibited a significantly higher specific IgG antibody activity compared to the other groups. Serum optical density (O.D.) values for PBD were 1.187 +/- 0.738 vs. 0.024 +/- 0.033, 0.255 +/- 0.471, and 0.204 +/- 0.346 for CHVS, AR and IPF, respectively (P < 0.05). Salivary O.D. for PBD were 0.801 +/- 0.447 vs 0.010 +/- 0.011, 0.104 +/- 0.151, and 0.22 +/- 0.447 (P < 0.05). In contrast, serum specific IgA did not discriminate between PBD and IPF patients. In addition, although the PBD group exhibited the highest values of IgA salivary APSA, high levels were also observed in saliva specimens from CHVS, a group of normal individuals who deny pigeon exposure. These findings suggest that measurement of IgG salivary APSA can play a role in the evaluation process of patients with pigeon breeder's disease.

Adult↗

PubMed1996

Correlation between pulmonary fibrosis and the lung pressure-volume curve.

The severity of pulmonary fibrosis is the main prognostic factor for survival of patients with interstitial lung diseases (ILD). Unfortunately, lung biopsy, which is the best method to assess fibrosis quantitatively, is done only once during the evolution of the disease. In this study we analyzed the relationship between the degree of fibrosis and the exponential constant k, derived from the lung pressure-volume curve (LPVC) in 33 patients with chronic ILD, 19 with pigeon breeder's disease (PBD), and 14 with idiopathic pulmonary fibrosis (IPF). Pulmonary function tests, including the LPVC, were obtained before biopsy. A semiquantitative histologic assessment of the severity of fibrosis was performed on lung tissues. All patients showed a decrease of total lung capacity, residual volume, compliance, and Pao2. The mean value of the constant k was 0.08 +/- 0.06. When expressed as a percent of normal values, 25 patients exhibited values of k lower than 70% of predicted; of the remaining 8 patients whose values were above 70% of predicted, 7 had PBD and only one IPF. On morphologic analysis, 19 patients displayed more than 50% fibrosis. No significant correlations were found between the extent of the lesion or severity of lung fibrosis and the conventional pulmonary function tests. By contrast, a moderate but significant correlation was found between k and the severity of lung fibrosis (r = -0.38, p < 0.05). These findings show that the shape of the LPVC, represented by the constant k, predicts the degree of lung fibrosis and could be useful in the clinical assessment and follow-up of patients with ILD.

Adolescent↗

PubMed1996

Cellular immune response to fractionated avian antigens by peripheral blood mononuclear cells from patients with pigeon breeder's disease.

Pigeon breeder's disease (PBD), a form of hypersensitivity pneumonitis caused by repeated inhalation of antigens of pigeon origin, is characterized by a diffuse inflammation of the lower respiratory tract. Although a variety of immunologic and nonimmunologic mechanisms have been described in the development of the disease, the pathogenesis is still far from clear. In this study we analyzed the T-lymphocyte proliferative response to a variety of avian antigens with use of peripheral blood mononuclear cells from 11 patients who had PBD and 10 healthy volunteers. We used a new method based on avian antigen-bearing nitrocellulose particles derived from Western blots to study the T-cell proliferative response to 15 antigenic fractions obtained from pigeon serum. With this technique, complex mixtures of antigens can be fractionated by polyacrylamide gel electrophoresis, transferred to nitrocellulose membranes, and used for T-cell proliferation assays with selected antigenic determinants. A wide variety of responses were observed, and there were no reproducible patterns of reaction within either group. Nine of 10 healthy subjects responded to some soluble fractions. However, patients with PBD displayed the strongest response and responded to a significantly greater number of antigenic fractions. Fraction 2, representing a 220 kd molecular weight protein, was the only immunodominant antigen when both groups were compared; it was recognized by 73% of the patients with PBD and by only 20% of control subjects (p < 0.03). These findings show that T lymphocytes of patients with PBD recognize a wide range of bird proteins, which induce marked T-cell proliferation.

Adult↗

PubMed1996

Tobacco smoke-induced lung emphysema in guinea pigs is associated with increased interstitial collagenase.

We examined the expression of interstitial collagenase and its enzymatic activity in lung damage induced by tobacco smoke. Guinea pigs were exposed to the smoke of 20 cigarettes per day from 1-8 wk. Age-matched guinea pigs were used as controls. At 6 and 8 wk of smoke exposure, lungs exhibited interstitial and peribronchiolar inflammation and moderate emphysematous changes. In situ hybridization of injured lungs revealed patchy expression of collagenase mRNA mainly in macrophages but also in alveolar epithelial and interstitial cells. Immunoreactive protein was detected in alveolar macrophages and in the alveolar walls and interstitium. Collagenolytic activity increased beginning in the 4th wk of exposure (0.7 +/- 0.43 micrograms collagen degraded/mg collagen incubated relative to 0.23 +/- 0.14 in controls; P < 0.05). At 6 and 8 wk, values were 0.85 +/- 0.34 and 0.98 +/- 0.33 compared with 0.25 +/- 0.11 and 0.26 +/- 13 in controls (P < 0.005 and 0.001). Collagen concentration decreased from 50.7 +/- 8.5 mg/g dry wt in control lungs to 40.2 +/- 5.0 and 42.9 +/- 6.0 at 6 and 8 wk of exposure, respectively (P < 0.05). These results strongly suggest that increased interstitial collagen degradation plays a role in the development of lung emphysema.

Animals↗

PubMed1996

Increased expression of intercellular adhesion molecule 1, CD11/CD18 cell surface adhesion glycoproteins and alpha 4 beta 1 integrin in a rat model of chronic interstitial lung fibrosis.

The expression of the intercellular adhesion molecule 1 (ICAM-1), and the integrins CD49, CD11b/c, and CD11a (LFA-1 alpha chain) was analyzed in an experimental model of pulmonary fibrosis. Adult rats were exposed to 75% oxygen during 10 weeks, and to 2.0 mg/kg of paraquat twice weekly. Rats were sacrificed at 2 days, and at 2 and 10 weeks after the first injection of paraquat. Lungs were fixed in 4% paraformaldehyde and used for histology and immunohistochemistry. At 2 days the lungs showed a diffuse inflammation composed of a mixed polymorphonuclear and mononuclear cell infiltrate. Afterwards, the inflammatory process was predominantly mononuclear, and an increasing fibroblast proliferation was observed. Early inflammatory events (48 h) correlated with a moderate increased expression of ICAM-1, LFA, and CD11b/c in epithelial cells as well as a pronounced expression of ICAM-1 and CD11b/c in macrophages. At 2 and 10 weeks, there was a progressive increased expression of CD11b/c and ICAM-1 by macrophages, as well as of LFA in epithelial cells, and of ICAM-1 and CD49 by epithelial and interstitial cells. Lymphocytes showed a slight increased expression of LFA at 2 weeks, and of CD49 at 2 and 10 weeks. These results suggest that macrophages expressing ICAM-1, CD11b/c, and CD49 are involved in the earlier and late phases of the disease whereas fibroblast and epithelial cells expressing ICAM-1 and CD49 might play a role in the cell interactions involved in the fibrotic phase.

Animals↗

PubMed1996

Exposure to biomass smoke and chronic airway disease in Mexican women. A case-control study.

A case-control study was performed in women older than 40 yr of age to evaluate the risk of cooking with traditional wood stoves for chronic bronchitis and chronic airway obstruction (CAO). The subjects were recruited from patients attending a referral chest hospital in Mexico City. We selected 127 patients with chronic bronchitis or CAO, of which 63 had chronic bronchitis alone, 23 had CAO alone (FEV1 less than 75% of predicted), and 41 had both chronic bronchitis and CAO (cases). Four control groups were selected: 83 patients with pulmonary tuberculosis, 100 patients with interstitial lung diseases, 97 patients with ear, nose and throat ailments, and 95 healthy visitors to the hospital (controls). Exposure to wood smoke, assessed as any or none, and as hour-years (years of exposure multiplied by average hours of exposure per day) was significantly higher in cases than in controls. Crude odds ratios for wood smoke exposure were 3.9 (95% CI, 2.0 to 7.6) for chronic bronchitis only, 9.7 (95% CI, 3.7 to 27) for CAO plus chronic bronchitis, and 1.8 (95% CI, 0.7 to 4.7) for CAO only. Differences in exposure to wood smoke persisted after adjusting by stratification and logistic regression for age, income, education, smoking, place of residence, and place of birth. Risk of chronic bronchitis alone and chronic bronchitis with CAO increased linearly with hour-years of cooking with a wood stove; odds ratios for exposure to more than 200 hour-years compared with nonexposed were 15.0 (95% CI, 5.6 to 40) for chronic bronchitis only and 75 (95% CI, 18 to 306) for chronic bronchitis with CAO. The findings support a causal role of domestic wood smoke exposure in chronic bronchitis and chronic airflow obstruction.

Adult↗

PubMed1996

Increased expression of gelatinases and collagenase in rat lungs exposed to 100% oxygen.

Exposure of adult rats to 100% O2 produces a lethal injury by 72 h. We reasoned that matrix metalloproteinases participate in the pathogenesis of hyperoxic lung injury. To that end we studied the expression and activity of gelatinases A and B and interstitial collagenase in lung tissues and bronchoalveolar lavage fluids (BALF) of rats exposed to 100% oxygen for 60 h. Gelatin zymography of BALF samples revealed a 472 kDa molecular species both in controls and oxygen-exposed animals. In addition, BALF from hyperoxic rats exhibited a 95-kDa gelatinase. Likewise, BALF total gelatinolytic and collagenolytic activities were significantly increased in oxygen-exposed rats. In situ hybridization revealed an increase in type IV collagenases as well as interstitial collagenase mRNAs in the oxygen-exposed lungs. The three enzymes were expressed by alveolar macrophages, and in variable degrees by interstitial and alveolar epithelial cells. Immunoreactive gelatinase B and collagenase paralleled the cell localization of the mRNAs but were also detected in the alveolar walls and interstitium. In situ zymography showed gelatinolytic activity in frozen sections of oxygen-exposed lungs but not in normal lungs. The upregulation of these metalloproteinases during acute exposure to 100% O2 suggests that they might contribute to hyperoxic lung damage through the degradation of extracellular matrix components.

Animals↗

PubMed1996

Bronchiolitis in chronic pigeon breeder's disease. Morphologic evidence of a spectrum of small airway lesions in hypersensitivity pneumonitis induced by avian antigens.

We analyzed 36 open lung biopsy specimens from patients with chronic pigeon breeder's disease (PBD) to assess bronchiolar involvement and its relationship to the parenchymal pathologic abnormalities. Likewise, 21 biopsy specimens obtained from patients with usual interstitial pneumonia (UIP) were also examined. The bronchiolar abnormalities were scored by the method of Wright et al using a panel of photographs. In addition, the severity of lung fibrosis was evaluated in all samples and expressed as percentage in multiples of ten. A variable degree of epithelial cell metaplasia, bronchiolar inflammation and fibrosis, smooth muscle hypertrophy, extrinsic small airways narrowing, and intraluminal macrophages was observed in both diseases. Occasionally, hyperplasia of lymphoid follicles was also present. Bronchiolar changes were proportional in type and severity to the parenchymal damage. Spearman's nonparametric correlation between fibrosis in parenchyma and fibrosis in membranous bronchiole for the complete group (including patients with UIP and with PBD) showed a moderate but significant association (R = 0.51; p < 0.01). A significant association was also demonstrated when the score for bronchiolar fibrosis and inflammation was evaluated in relation to lung fibrosis divided in high degree (> 50%) and low degree (< 50%), respectively. In the case of patients with PBD, the correlation between bronchiolar and parenchymatous fibrosis was of 0.33 (p < 0.05). In general, bronchiolar fibrosis was less severe and inflammation more severe in PBD lungs compared with patients with UIP. Fibrosis in membranous bronchioles correlated with increased mortality in the complete group of patients, but the impact on mortality disappeared after correcting for overall fibrosis in the biopsy sample. Our findings demonstrate that a spectrum of bronchiolar lesions is usually observed in chronic PBD lungs, although the predominant pattern is similar to that found in the surrounding parenchyma, suggesting that the damage occurs in parallel.

Adult↗

PubMed1996

Matrix metalloproteinases and lung injury.

The dynamic equilibrium of extracellular matrix (ECM) under different physiological conditions is a consequence of the balance between the regulation of synthesis and degradation of ECM components. Matrix metalloproteinases (MMPs), a family of structurally related zinc-dependent endopeptidases, are the physiological mediators of matrix remodeling. The expression and activity of these enzymes are highly regulated at several intra- and extracellular levels, so that in vivo enzymatic activity is the final result of a complex series of events including gene expression, zymogen activation, matrix binding, and enzymatic inhibition. MMPs are expressed at low levels in normal adult tissues, and their upregulation appears to play an important role in the development of a number of pathological processes. In acute lung injury, a disorder characterized by a severe disruption of the gas exchange alveolo-capillary structures, the upregulation of interstitial collagenase and gelatinases A and B strongly suggests that MMPs contribute to acute lung damage by facilitating the migration of inflammatory cells, as well as to the disruption of basement membrane components and extracellular matrix remodeling.

Extracellular Matrix↗

PubMed1996

Pathogenic mechanisms in the development of diffuse pulmonary fibrosis.

Diffuse pulmonary fibrosis is characterized by abnormal proliferation of mesenchymal cells, specifically fibroblasts and myofibroblasts, and by the accumulation of excessive amounts of matrix proteins, mainly collagens. The development of this pathological process is preceded by an inflammatory response, often dominated by macrophages and lymphocytes, which is mediated by the local release of chemoattractant factors, acting coordinately with an upregulation of cell-surface adhesion molecules. A subsequent persisting fibroproliferative reaction, in both interstitial and intraalveolar spaces, with progressive collagen accumulation distorts the lung architecture irreversibly. Excessive collagen deposition is the result of an imbalance in the collagen turnover rates characterized by a transient increase in collagen synthesis and a decrease in collagen degradation. Fibrosis is considered otherwise to be the final common pathway of a variety of lung disorders, and in this context, the diagnosis of pulmonary fibrosis implies the recognition of an advanced stage in the evolution of a complex process of abnormal repair.

Cell Division↗

PubMed1995

Collagen metabolism in human aqueous humor from primary open-angle glaucoma. Decreased degradation and increased biosynthesis play a role in its pathogenesis.

OBJECTIVE: To explore the influence of aqueous humor from patients with glaucoma on collagen turnover. METHODS: The aqueous humor of patients with primary open-angle glaucoma (POAG), chronic angle-closure glaucoma, congenital glaucoma, neovascular glaucoma, and senile cataract (control group) was analyzed for its capacity to induce fibroblast proliferation, collagen synthesis, collagenolytic activity, and production of tissue inhibitor of metalloproteinase-1. All data were analyzed using the Mann-Whitney U test. RESULTS: Aqueous humor derived from patients with POAG induced a significant decrease of functional collagenase activity (mean +/- SE, 9.12 +/- 1.33 microgram of degraded collagen per milligram of incubated protein vs 20.94 +/- 4.14 micrograms from the control group, P < .05). The enzymatic activity in the other types of glaucoma was similar to that of controls. The POAG samples had a significantly higher concentration of tissue inhibitor of metalloproteinase-1 (mean +/- SE, 3.11 +/- 0.58 vs 0.91 +/- 0.13 micrograms/mL from controls; P < .05). The amount of immunoreactive tissue inhibitor of metalloproteinase-1 found in the other three groups was not significantly different from the control. Aqueous humor stimulated fibroblast proliferation in all cases, but significant differences were not observed between the POAG samples (mean +/- SE, 20,285 +/- 4642 cpm/mg of incubated protein) and the control group samples (26,550 +/- 3688 cpm/mg of incubated protein). Primary open-angle glaucoma fluids increased collagen synthesis significantly compared with the control group (mean +/- SD, 3352 +/- 630 vs 985 +/- 285, P < .05), and the other groups. CONCLUSIONS: An increase of collagen synthesis and a decrease of collagen degradation may contribute to an excessive deposit of collagen with loss of the trabecular cells during the development of POAG, and aqueous humor must be considered as a microenvironment that affects the metabolism or function of the trabecular meshwork or both.

Adult↗

PubMed1995

Inhaled Bordetella pertussis vaccine decreases airway responsiveness in guinea pigs.

Bordetella pertussis (BP) has been used as adjuvant for experimental animal immunization, but its effects on airway responsiveness are uncertain. Three groups of guinea pigs were used: animals with a single exposure to inhaled BP vaccine (strain 134, total dose 1.24 x 10(12) germs), animals submitted to a sensitization procedure through inhalation of ovalbumin plus BP, and healthy control animals. Four weeks after inhalation of BP or after the beginning of sensitization, dose- or concentration-response curves to histamine were constructed in vivo and in vitro (tracheal and parenchymal preparations). We found that BP alone produced lower responses to histamine than control guinea pigs in vivo (insufflation pressure, p = 0.0003) and in tracheal tissues (p = 0.04), but not in parenchymal preparations. Sensitization did not modify the responsiveness compared with their respective controls. These results suggest that some BP component(s), probably pertussis toxin, causes a long lasting airway hyporesponsiveness in guinea pigs.

Adjuvants, Immunologic↗

PubMed1995

Influence on collagen metabolism of vitreous from eyes with proliferative vitreoretinopathy.

PURPOSE: Proliferative vitreoretinopathy (PVR) is characterized by cell proliferation and membrane formation on the vitreoretinal cavity of the eye. The membranes are composed of extracellular matrix, mainly collagen type I. To explore the possible mechanisms involved in PVR membrane formation, the authors analyzed the role of vitreous humor on collagen turnover. METHODS: The authors studied vitreous samples from ten patients with PVR and from five donor eyes (keratoplasty) as the control group. Human lung fibroblasts were used to study the influence of vitreous on collagen synthesis and cell proliferation. Neutralizing antibodies against transforming growth factor-beta 2 (TGF-beta 2) were used to inhibit the fibroblast collagen synthesis induced by the vitreous samples. Collagenolytic activity was analyzed in vitreous fluid using 3H-labeled collagen. RESULTS: The authors found that samples obtained from patients with PVR significantly increased collagen synthesis (2979 +/- 963.26 versus 800 +/- 232 dpm of 3H-proline incorporated per milligram of vitreous-incubated protein; P < 0.00043), without affecting fibroblast replication. The collagen synthesis induced by the vitreous samples was inhibited by anti-TGF-beta 2 antibodies in both groups (0 and 481 +/- 59 dpm of 3H-proline incorporated per milligram of vitreous-incubated protein for control and PVR samples, respectively). Collagenolytic activity was considerably lower in vitreous derived from PVR samples compared with the control group (19.9 +/- 20.3 versus 234.1 +/- 19.1 micrograms of degraded collagen per milligram of vitreous-incubated protein; P < 0.0032). CONCLUSION: These results suggest that a combined mechanism, including an increase of collagen synthesis mediated at least in part by TGF-beta 2 and a decrease of collagen degradation, may contribute to the exaggerated deposition of collagen observed in PVR membranes, and that vitreous should be considered as a part of the microenvironment that is participating actively in the pathogenesis of this vitreoretinal disorder.

Cell Division↗

PubMed1995

Fibroblasts isolated after fibrotic lung injury induce apoptosis of alveolar epithelial cells in vitro.

Primary lung fibroblasts were isolated from patients with idiopathic pulmonary fibrosis (HIPF), from normal human lung tissue (NH), from rats treated with 75% oxygen and paraquat (PA), and from normal adult rats (NR). Serum-free media conditioned by each fibroblast strain were tested on the human A549 cell line (HIPF and NH media) or on primary alveolar epithelial cells (AEC) isolated from normal adult rats (PA or NR media). Over 20-h incubation, HIPF- or PA-conditioned media induced DNA fragmentation and significant decreases in total recoverable DNA and cell number of A549 or AEC, respectively; NH or NR media had no significant effect relative to serum-free unconditioned media. Apoptosis of A549 and AEC was detected by altered nuclear morphology and was confirmed by terminal deoxynucleotidyl transferase-mediated bio-dUTP nick end labeling. The endonuclease inhibitors 10 microM aurintricarboxylic acid and 50 microM zinc inhibited HIPF-induced apoptosis of A549 cells by 68 and 71%, respectively. Both apoptosis and necrosis were induced by HIPF and PA media in a concentration-dependent manner. These results suggest that altered fibroblasts emerging during fibrotic lung injury release a soluble factor(s) capable of inducing cell death and net loss of AEC.

Animals↗

PubMed1995

Reversal of digital clubbing after lung transplantation.

Digital clubbing is a common sign in a variety of lung diseases. Although its pathogenesis remains unclear, it is known that the degree of clubbing might vary and even disappear, particularly when the underlying disease is a malignant neoplasm that has been removed. By contrast, because of the short expectancy of life in patients with pulmonary fibrosis, it is unusual to observe regression of clubbing. In this work, we report a case of reversible clubbing after lung transplantation.

Adult↗

PubMed1995

Expression of a 2.8-kb PDGF-B/c-sis transcript and synthesis of PDGF-like protein by human lung fibroblasts.

The replication of fibroblasts is thought to be controlled by exogenous growth factors mainly secreted by macrophages and epithelial cells. However, under standard culture conditions, lung fibroblasts are able to produce several growth factors, suggesting an autocrine pathway of proliferation. In this work, we examined the expression of platelet-derived growth factor (PDGF-A) and PDGF-B-messenger RNA (mRNAs) by fibroblasts derived from four human adult normal lungs and from two fibrotic lungs. Northern blot analysis showed that both normal and idiopathic pulmonary fibrosis (IPF)-derived fibroblasts expressed a 2.8 PDGF-B/c-sis mRNA. This transcript was also observed as a minor form in human osteosarcoma cell line, used as control, which predominantly expressed a 4.0-kb PDGF-B mRNA. In two fibroblast cell lines, one fibrotic and one normal, the 4.0-kb transcript was also observed but was always weaker than the 2.8-kb mRNA. PDGF-A mRNA was not detected. By immunofluorescence, lung fibroblasts exhibited intracytoplasmic PDGF-like protein. Likewise, conditioned media from normal and IPF lung fibroblasts stimulated 3H-thymidine incorporation in BALB/c-3T3 cells that was significantly inhibited by anti-PDGF antibody. These results show that in vitro, some human lung fibroblasts express PDGF-B/c-sis mRNA, mainly an alternate 2.8-kb transcript, and produce PDGF-like protein.

Blotting, Northern↗