Biomedical subjects

L Yin

Publications and source records attributed to L Yin.

At least 73 records · Page 4Linked to original sources

PubMed2000

The luminal short-chain fatty acid butyrate modulates NF-kappaB activity in a human colonic epithelial cell line.

BACKGROUND & AIMS: The transcription factor nuclear factor-kappaB (NF-kappaB) plays a central role in regulating immune and inflammatory responses. Because butyrate deficiency has been associated with inflammatory bowel disease, we examined the effect of butyrate on NF-kappaB activity in the human HT-29 colonic cell line. METHODS: The influence of butyrate (4 mmol/L) on NF-kappaB activity was determined using the gel mobility shift assay. The effect of butyrate on the expression of NF-kappaB subunits and inhibitory proteins was determined by immunoblotting. NF-kappaB-regulated gene expression was assayed by primer extension of intercellular adhesion molecule 1 and Mn superoxide dismutase messenger RNA, and by analysis of a transfected luciferase reporter. RESULTS: Exposure of HT-29 cells to butyrate eliminated their constitutive NF-kappaB, p50 dimer activity. This inhibition corresponded with a reduction in p50 nuclear localization, without a reduction in expression. Butyrate also selectively modulated activation of NF-kappaB, suppressing its activation by tumor necrosis factor alpha and phorbol ester more than 10-fold, without affecting the activity induced by interleukin (IL)-1beta. Butyrate did, however, enhance formation of the stronger p65-p50 transcriptional activator in IL-1beta-stimulated cells. The changes in NF-kappaB activation did not correlate with changes in IkappaBalpha levels. Gene expression reflected DNA binding. The influence of butyrate on NF-kappaB may result in part from its ability to inhibit deacetylases because the specific deacetylase inhibitor trichostatin A has a similar effect. CONCLUSIONS: These findings suggest that the influences of butyrate on colonic inflammatory responses may result in part from its influence on NF-kappaB activation. This activity of butyrate apparently involves its ability to inhibit deacetylases.

Acetylation↗

PubMed2000

Dose-finding study of valspodar (PSC 833) with daunorubicin and cytarabine to reverse multidrug resistance in elderly patients with previously untreated acute myeloid leukemia.

INTRODUCTION: This trial was designed to determine the maximum tolerated dose of intravenous daunorubicin (DNR) in combination with valspodar and to test the feasibility of P-glycoprotein modulation using valspodar in elderly patients with previously untreated acute myelogenous leukemia receiving standard induction chemotherapy. METHODS: Patients > or =60 years of age with previously untreated AML received valspodar (10 mg/kg/24 h by continuous intravenous infusion [CIV] on days 1-4 with a 2-mg/kg loading dose on day 1) in conjunction with two cycles of induction chemotherapy consisting of cytarabine (200 mg/m(2) CIV on days 1-7), and DNR (35 mg/m(2) [cohort 1] or 45 mg/m(2) [cohort 2] on days 1-3, intravenous bolus). Patients were assessed for dose-limiting toxicities (DLT), response rate, event-free and overall survival, and pharmacokinetics of valspodar and DNR. RESULTS: Valspodar was well tolerated at the lower DNR dose level (ie, 35 mg/m(2)) resulting in a 21% rate of DLT and only three toxic deaths. Treatment-related mortality was unacceptably high at the 45 mg/m(2) DNR dose level. The complete response rate was 49% overall and similar in both cohorts. The median overall survival of patients was 333 days in cohort 1 compared to 98 days in cohort 2. At baseline, 70% of assessable patients were P-glycoprotein positive. CONCLUSION: Substantial inhibition of P-glycoprotein activity can be achieved in this patient population at clinically tolerable doses of valspodar and DNR. The maximum tolerated dose of DNR was established as 35 mg/m(2). This regimen is being further evaluated in phase III trials.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2000

Proliferation of hepatic lineage cells of normal C57BL and interleukin-6 knockout mice after cocaine-induced periportal injury.

The cellular response to periportal liver injury, induced by phenobarbital feeding and cocaine injection, is used to compare the restitutive proliferation of hepatocytes, cholangiocytes, and oval cells in the livers of normal control to those of interleukin-6 (IL-6) knockout mice. After this injury hepatocytes in noninjured middle and central zones start to proliferate first, followed by proliferation of cholangiocytes and intraportal oval cells. Proliferation of all cell types peaks at 2 days, but oval cells continue to proliferate and differentiate through days 4 and 6 as they reconstitute the necrotic zone. By day 10, the injured zone is completely repaired, and no dividing cells remain. During the first 3 to 4 days after injury, the number of proliferating hepatocytes, cholangiocytes, and sinusoidal cells is lower in IL-6 knockout mice than in normal mice, whereas the number of dividing oval cells is higher. However, overall repair of the injury is accomplished in the same time period in both groups. During repair of the periportal zone, oval cells acquire differentiation markers of hepatocytes as they cross the zone of injury. In conclusion, the phenobarbital/cocaine injury model is useful to study restitutive proliferation of mouse liver cell lineages. The proliferative response in IL-6 knockout mice shows that IL-6 is not required for proliferation of liver cells; timely repair of liver injury occurs in both normal and IL-6 knockout mice. Increased proliferation of oval cells in IL-6 knockout mice may compensate for the lower proliferation of other liver cell types.

Alanine Transaminase↗

PubMed2000

Otolaryngology consultation for peritonsillar abscess in the pediatric population.

OBJECTIVE: To assess clinical outcomes of children seen in consultation for peritonsillar abscess treated without the routine use of computed tomography or needle aspiration. STUDY DESIGN: Retrospective review of patients evaluated in the emergency department for possible peritonsillar abscess. Patient outcomes are reviewed with a statistical analysis of children grouped according to age. METHODS: A series of 102 patients, ages 8 months to 19 years, who were evaluated by the emergency department with otolaryngology consultation for possible peritonsillar abscess. All patients were admitted and given intravenous fluid replacement, antibiotics, and analgesia. Patients who responded to 24 hours of medical treatment were discharged, whereas patients who did not respond underwent elective tonsillectomy. MAIN OUTCOME MEASURE: Outcome of patients evaluated for peritonsillar abscess treated without immediate surgery, needle aspiration, or computed tomography. Outcomes are correlated with age and clinical findings. RESULTS: Fifty-two patients were discharged after initial medical therapy. Fifty patients underwent elective tonsillectomy; 40 of these patients were found to have abscesses at the time of surgery. When analyzed according to age, patients ages 8 months to 6 years were more likely to respond to medical treatment than children ages 7 to 12 and 12 to 19 (P = .023). Significant differences in the mean age of children requiring surgery (11.0 y) compared with those who responded to medical treatment (7.9 y) were observed (P = .003). Younger children who underwent tonsillectomy had a lower incidence of surgically confirmed abscess. CONCLUSIONS: A significant number of children presenting with odynophagia, malaise, pharyngotonsillar bulge, and decreased oral intake respond to medical therapy without radiological evaluation or surgical intervention. Additionally, younger children (1-6 y) are more likely to respond to medical treatment than older children. Pertinent clinical data, as well as advantages and disadvantages of this approach, are discussed.

Adolescent↗

PubMed2000

RET rearrangements in papillary thyroid carcinomas and adenomas detected by interphase FISH.

Activation of the RET protooncogene through somatic rearrangements represents the most common genetic alteration in papillary thyroid carcinoma (PTC). Three main rearranged forms of RET have been described: RET/PTC1 and RET/PTC3, which arise from a paracentric inversion of the long arm of chromosome 10, and RET/PTC2, which originates from a 10;17 translocation. We have developed a dual-color FISH approach to detect RET/PTC rearrangements in interphase nuclei of thyroid lesions. By using a pool of three cosmids encompassing the RET chromosome region and a chromosome 10 centromeric probe, we could discriminate between the presence of an inversion (RET/PTC1 and RET/PTC3) or a translocation (RET/PTC2). We have investigated a series of thyroid tissue samples from Italian and French patients corresponding to a total of 69 PTCs and 22 benign lesions. Among PTCs, 13 (18.8%) showed a RET rearrangement, and 11 (15.9%) of these carried an inversion (RET/PTC1 or RET/PTC3) in more than 10% of the nuclei examined. Activated forms of RET were also observed in three adenomas. RT-PCR analysis on the same samples confirmed the presence and the type of rearrangement predicted using FISH analysis. An interesting difference in the frequency and type of RET rearrangements was detected between the Italian and the French patients. Furthermore, we identified a putative novel type of rearrangement in at least one PTC sample. Several PTCs carried a significant number of cells characterized by a trisomy or a tetrasomy of chromosome 10. Overall, the FISH approach in interphase nuclei represents a powerful tool for detecting, at the single cell level, RET/PTC rearrangements and other anomalies involving the RET chromosome region.

Adenoma↗

PubMed2000

Myocardial contraction maps using tissue Doppler acceleration imaging.

OBJECTIVE: To evaluate the tissue Doppler acceleration imaging (TDAI) data which can be used to determine the intramural site of origin of myocardial contraction in response to electrical stimulation. METHODS: Six open-chest pigs with left ventricle (LV) pacing were evaluated with TDAI. An epicardial surface scanning method was used to collect short-axis views of the left ventricle. The electrode was implanted from the epicardium through the anterior free wall to an intramural position. RESULTS: During pacing, the intramural onset of myocardial acceleration occurred within 33 ms after electrical stimulation and always surrounded the embedded subendocardial end of the pacing needle. The observed short-axis diameter of the area of initial myocardial acceleration ranged from 2.9 mm to 5.0 mm (4.2 +/- 0.9 mm, n = 6). The onset of myocardial acceleration allowed appreciation of the initial intramural myocardial contraction. The spatial size and acceleration magnitude of the initial myocardial acceleration distribution were irregular. CONCLUSION: Two-dimensional myocardial acceleration mapping can show the intramural site of origin of myocardial contraction in response to paced electrical stimulation. The location of myocardial acceleration conformed to the site of initial electrical stimulation. The delay to the earliest regional myocardial contraction, 33 ms after paced electrical stimulation, was related to the frame rate of image acquisition.

Animals↗

PubMed1999

Cytolytic T lymphocyte-associated antigen-4 and the TCR zeta/CD3 complex, but not CD28, interact with clathrin adaptor complexes AP-1 and AP-2.

The negative signaling receptor cytolytic T lymphocyte-associated Ag-4 (CTLA-4) resides primarily in intracellular compartments such as the Golgi apparatus of T cells. However, little is known regarding the molecular mechanisms that influence this accumulation. In this study, we demonstrate binding of the clathrin adaptor complex AP-1 with the GVYVKM motif of the cytoplasmic domain of CTLA-4. Binding occurred primarily in the Golgi compartment of T cells, unlike with AP-2 binding that occurs mostly with cell surface CTLA-4. Although evidence was not found to implicate AP-1 binding in the retention of CTLA-4 in the Golgi, AP-1 appears to play a role in shuttling of excess receptor from the Golgi to the lysosomal compartments for degradation. In support of this, increased CTLA-4 synthesis resulted in an increase in CTLA-4/AP-1 binding and a concomitant increase in the appearance of CTLA-4 in the lysosomal compartment. At the same time, the level of intracellular receptor was maintained at a constant level, suggesting that CTLA-4/AP-1 binding represents one mechanism to ensure steady state levels of intracellular CTLA-4 in T cells. Finally, we demonstrate that the TCR zeta/CD3 complex (but not CD28) also binds to AP-1 and AP-2 complexes, thus providing a possible link between these two receptors in the regulation of T cell function.

Abatacept↗

PubMed1999

Spontaneous regression of primary autoreactivity during chronic progression of experimental autoimmune encephalomyelitis and multiple sclerosis.

Experimental autoimmune encephalomyelitis (EAE) is a widely used animal model for multiple sclerosis (MS). EAE is typically initiated by CD4(+) T helper cell type 1 (Th1) autoreactivity directed against a single priming immunodominant myelin peptide determinant. Recent studies have shown that clinical progression of EAE involves the accumulation of neo-autoreactivity, commonly referred to as epitope spreading, directed against peptide determinants not involved in the priming process. This study directly addresses the relative roles of primary autoreactivity and secondary epitope spreading in the progression of both EAE and MS. To this end we serially evaluated the development of several epitope-spreading cascades in SWXJ mice primed with distinctly different encephalitogenic determinants of myelin proteolipid protein. In a series of analogous experiments, we examined the development of epitope spreading in patients with isolated monosymptomatic demyelinating syndrome as their disease progressed to clinically definite MS. Our results indicate that in both EAE and MS, primary proliferative autoreactivity associated with onset of clinical disease invariably regresses with time and is often undetectable during periods of disease progression. In contrast, the emergence of sustained secondary autoreactivity to spreading determinants is consistently associated with disease progression in both EAE and MS. Our results indicate that chronic progression of EAE and MS involves a shifting of autoreactivity from primary initiating self-determinants to defined cascades of secondary determinants that sustain the self-recognition process during disease progression.

Acute Disease↗

PubMed1999

Th2 T cells expressing transgene PDGF-A serve as vectors for gene therapy in autoimmune demyelinating disease.

We hypothesized that T cells can be genetically modified to express growth factor transgene products capable of inducing oligodendrocyte progenitor proliferation. Autoreactive T cells isolated from SWXJ mice immunized with the p139-151 determinant of myelin proteolipid protein (PLP) were transfected with an antigen-inducible transgene for platelet-derived growth factor-A (PDGF), a growth factor important in regulating the development of oligodendrocytes. Isolated antigen-specific T cell clones expressed the PDGF transgene when stimulated with PLP 139-151 peptide and produced biologically active PDGF capable of inducing proliferation of oligodendrocyte progenitor cells. Furthermore, upon adoptive transfer, the PDGF transfected T cells migrated to the CNS and ameliorated ongoing disease. Our data indicate that autoreactive memory Th2 cells can be genetically modified so that upon engagement with self antigen they produce regenerative growth factors capable of mediating tissue repair during autoimmune disease.

Adoptive Transfer↗

PubMed1999

Regression and spreading of self-recognition during the development of autoimmune demyelinating disease.

The autoimmune T cell repertoire in experimental autoimmune encephalomyelitis (EAE) and multiple sclerosis (MS) is characterized by CD4(+)T cells of the Th1 phenotype that recognize peptide determinants of central nervous system (CNS) myelin proteins in an MHC class II-restricted manner. Our recent studies and those performed by others have shown that progression to chronicity in EAE and MS is accompanied by a broadening of the T cell repertoire with time. This acquired neo-autoreactivity is commonly referred to as epitope spreading and is presumably the result of endogenous priming to new self-determinants during the CNS inflammation that accompanies disease onset and relapse. In the present study we extend our earlier observations by showing that disease progression in both EAE and MS is accompanied by two concurrent events, viz. (1) the spontaneous regression of the primary established autoimmune repertoire associated with disease onset, and (2) the emergence of the epitope spreading cascade associated with disease progression. Our data show that disease initiation and disease progression in both EAE and MS are typically associated with distinctly different autoimmune T cell repertoires. Our data support the view that the natural development of self-recognition during autoimmune disease may best be understood when considered in the temporal context of an 'epitope du jour' and 'moving target' perspective.

Amino Acid Sequence↗

PubMed1999

Local intra-arterial fibrinolysis without arterial occlusion?

Local intra-arterial fibrinolysis (LIF) is the best choice at present for treatment of acute vessel occlusion in the vertebrobasilar territory and also, in selected cases, in the carotid territory. In almost all cases angiography demonstrates the site of occlusion exactly and gives information about collateral circulation. Contrary to this common approach, we report five patients with severe acute thromboembolic stroke in whom angiography revealed no occlusion of relevant arteries or their main branches. Under the hypothesis of persisting occlusion of perforating arteries to the brain stem we performed LIF in patients with a clinical basilar artery syndrome. Outcome in all but one of them was good following LIF. The clinical details are described and possible reasons discussed.

Adult↗

PubMed1999

SH2D1A mutation analysis for diagnosis of XLP in typical and atypical patients.

X-linked lymphoproliferative disease (XLP) is a rare inherited immunodeficiency to Epstein-Barr virus (EBV). The gene responsible for XLP has recently been identified as the four-exon SH2D1A gene encoding a 128-amino-acid protein that contains an SH2-domain. Functional studies indicate the SH2D1A protein acts as a regulator of at least two signal transduction pathways initiated by the cell surface molecules SLAM and 2B4, respectively, and possibly related to the host immune response to EBV infection. We have carried out a systematic mutation study of the SH2D1A gene in our series of 19 typical and 8 atypical XLP patients by polymerase chain reaction (PCR), reverse transcription/PCR, and sequencing, and have reconstructed the haplotypes of the patients. Four out of the 13 mutations detected are previously unreported. The identification of SH2D1A mutations in carriers from all three XLP families screened and the detection of mutations in two out of eight atypical patients indicates the usefulness of a DNA-based diagnosis for XLP disease.

Carrier Proteins↗

PubMed1999

Participation of different cell types in the restitutive response of the rat liver to periportal injury induced by allyl alcohol.

BACKGROUND/AIM: Restitution of periportal liver necrosis induced by allyl alcohol involves proliferation and differentiation of putative liver stem cells. The participation of different non-epithelial cell types required to restore the liver cord structure in this process has not been well documented. The aim of the study was to determine the anatomic relationships among cells of liver lineage, extracellular matrix, and non-parenchymal cells during repair of periportal liver injury. METHODS: Periportal liver injury in rats was induced by intraperitoneal injection of allyl alcohol. Cells of the liver lineage, as well as Kupffer cells, hepatic stellate cells, macrophages, and the extracellular matrix components fibronectin and laminin were localized using immunohistologic methods for 7 days after injury. RESULTS: During the first day there was loss of periportal hepatocytes, as well as sinusoidal nonparenchymal cells, including macrophages, Kupffer cells and hepatic stellate cells. After day 1 macrophages appeared within the necrotic zone, increased until days 3-4, and then decreased to a few cells within reappearing sinusoids. At days 2-5 there was first proliferation of small "null" intraportal cells, which later acquired markers of ductular (OV-6, CKPan ) and liver cell differentiation (alphafetoprotein, carbamoylphosphate synthetase-I), eventually assuming mature hepatocyte morphology. There was also moderate bile duct hyperplasia with extension of small newly-formed ducts from the intraportal zone into the immediate periportal zone. Kupffer cells and hepatic stellate cells became enlarged at the borders of the necrotic and non-necrotic central zone and then appeared to migrate into the oval cell population expanding across the periportal zone. During the restitution phase, hepatic stellate cells were closely associated with the proliferating oval cells, surrounding small aggregates of oval cells which appeared to be forming liver cords. Kupffer cells also stained for fibronectin, and fibronectin was seen at the intersection of the injured portal and uninjured central zones and around the expanding oval cells. In some intraportal zones, the laminin surrounding the bile ducts was lost. It was speculated that this may permit proliferating ductular cells to migrate out of the bile ducts into the periportal zone. By days 6 and 7 most of the injured liver was restored to normal, with a few foci of chronic inflammation remaining. CONCLUSIONS: There is a close anatomic relationship between immature liver lineage cells (oval/duct cells) and non-parenchymal cells during the restitutive repair of periportal injury. The nature of this relationship to the possible production of growth factors and expression of growth factor receptors by the cells involved during the restitution process is discussed.

Animals↗

PubMed1999

Ventilatory, lactate-derived and catecholamine thresholds during incremental treadmill running: relationship and reproducibility.

Anaerobic threshold as a basic criterion of training recommendation can be estimated by various parameters. The purpose of this study was to investigate the relationship and the reproducibility of ventilatory, lactate-derived and catecholamine thresholds of an incremental treadmill exercise. Therefore, 11 male subjects underwent two incremental treadmill tests within 7 days. The lactate threshold (LT) was determined at the lowest value of the lactate-equivalent (ratio lactate/performance). The individual anaerobic threshold (IAT) was calculated at LT+1.5 mmol/L lactate. The ventilatory thresholds, using mass-spectrometry, were defined by the V-slope method (AT) and at the deflection point of end-tidal CO2 (ET-CO2) concentration (RCP). The thresholds of epinephrine (TE) and norepinephrine (TNE) were calculated in the manner of LT. The running velocities were highly reproducible at LT (test-retest correlation coefficient r=0.90), IAT (r=0.97), AT (r=0.88) and RCP (r=0.95). By contrast TE (r=0.49) and TNE (r=0.46) showed a poor reproducibility. TE and TNE occurred 5-11% below LT and AT with a low correlation to LT and AT. LT was found 4% below AT, both were correlated with r=0.70 (p<0.01, test 1) and r=0.95 (p<0.01, test 2). IAT occurred 7-8% above RCP, in both tests a close correlation was found between IAT and RCP of r=0.97 (p<0.01). In summary, the ventilatory and lactate-derived thresholds show a high and similar reproducibility, but the catecholamine threshold does not. In the present exercise protocol, there are systematic differences between the lactate-derived and ventilatory thresholds, in spite of a close relationship, and these must be taken into account in recommendations derived for training.

Adult↗

PubMed1999

[Lipopolysaccharide-induced apoptosis of rat hepatocyte in vitro].

OBJECTIVES: To investigate the effect of lipopolysaccharide(LPS) on hepatocyte in vitro. METHODS: The hepatocytes were isolated in the way of liver perfusion with 0.05% collagenase type I and type IV, and cultured for 24 h in vitro before LPS was added directly into the culturing medium. Propidium iodide(PI) staining, and transmission electron microscopy techniques had been used to observe the morphological changes of hepatocyte treated with LPS. DNA-fragment assay was analyzed by the agarose gel electrophoresis to determine apoptotic level. RESULTS: Hepatocytes incubated with LPS exhibited some typical apoptosis-specific morphological features. The DNA-fragment by agarose gel electrophoresis demonstrated the typical ladder pattern on the hepatocytes directly exposed to LPS, but it was absent in the group used ATA, an inhibitor of apoptosis. These morphological changes, accompanied by DNA fragmentation assay, confirmed that cells were dying through an apoptotic pathway. In addition, the hepatocyte number of apoptosis increased parallel with the dose of LPS and time within 24 h when hepatocytes were exposed to LPS alone. CONCLUSIONS: LPS can induce apoptosis of hepatocyte in vitro.

Animals↗

PubMed1999

Flow cytometric analysis of the toxicity of nitrofen in cultured keratinocytes.

Lactate dehydrogenase (LDH) release test, 3H-thymidine (3H-TdR) and 3H-leucine (3H-Leu) incorporation tests and flow cytometric analysis (FCM) of cell cycle were employed to elucidate cellular and molecular mechanism of nitrofen-induced toxicity in cultured keratinocytes. The results showed that cell morphologic damages were observed after exposure to 1.0 mmol/L and 10.0 mmol/L nitrofen. LDH release increased in a dose- and time-dependent manner. Depressions in 3H-TdR and 3H-Leu incorporation were found even at 0.01 mmol/L, and increased with the exposure dose. Cell cycle was analyzed from the DNA- histogram with propidium iodide stain. The results showed that there was no pronounced alteration in cell cycle after cells exposed to 0.01 and 0.1 mmol/L nitrofen. At dose of 1.0 mmol/L, S phase cells increased 2 times of that of control. With the increase of dose, G2/M phase cells became to increase about 5 times of that of the control. At 1.0 mmol/L, time course of cell cycle after exposure was observed. At the beginning of exposure, cells in S phase and G2/M phase were about 8.7% and 11%. Following 24 h incubation with nitrofen, cells in S phase increased to 18.0% with almost no change in G2/M. 72 h after exposure, G2/M phase cells increased to 63.3%. The above results demonstrated that S phase and G2/M phase blockage in cultured keratinocytes after exposed to nitrofen seems of importance in the mechanism of nitrofen-induced toxicity.

Animals↗

PubMed1999

Ureaplasma urealyticum infection and apoptosis of spermatogenic cells.

AIM: To study the relationship between Ureaplasma urealyticum (UU) infection and apoptosis of human spermatogenic cells. METHODS: Spermatogenic cells were observed under light microscope with Wright-Giemsa staining and by means of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate (dUTP)-biotin nick-end labeling (TUNEL) technique. RESULTS: Apoptotic rate of UU-infected males (15.5% +/- 6.8%) was significantly higher than that of controls (5.2% +/- 2.3%). CONCLUSION: Apoptosis of spermatogenic cells can be caused by UU infection, which provides further evidence for UU-induced male infertility.

Adult↗

PubMed1999

Correlation of cell proliferation inhibition and apoptosis induction with expression of human beta 5 integrin on hematopoietic cells.

OBJECTIVE: To investigate the function of the alpha v beta 5 integrin in hematopoietic cells. METHODS: Tissue culture, integrin expression vectors, gene transfer, polymerase chain reaction (PCR), apoptosis analyses and cytometic analysis were made on hematopoietic cells. RESULTS: The beta 5 integrin cDNA was not expressed in hematopoietic cells following exposure to the beta 5 integrin retrovirus vector pG beta 5CHT. Unbalanced expression of the alpha v beta 3 and alpha v beta 5 integrins occurred during apoptosis induced by serum depletion and upon differentiation. The treatment of hematopoietic cells with anti-alpha v beta 5 monoclonal antibody inhibited apoptosis induced by serum depletion. Inducible expression of the beta 5 integrin cDNA in the hematopoietic cell line K562 caused cellular proliferation inhibition. CONCLUSION: The alpha v beta 5 integrin cDNA in hematopoietic cells can inhibit the proliferation of the hematopoietic cell, cause the differentiation of the hematopoietic cells and induce the apoptosis of the hematopoietic cells.

Apoptosis↗