Search PubMed⌕ Search

Biomedical subjects

K Sueishi

Publications and source records attributed to K Sueishi.

At least 37 records · Page 2Linked to original sources
PubMed2001

Clinicopathological and molecular evidence indicating the independence of bronchioloalveolar components from other subtypes of human peripheral lung adenocarcinoma.

Although human lung adenocarcinoma has diverse histological subtypes, the correlation between histological subtypes and occurrence of the p53 gene mutation has been given less attention. We investigated 145 surgically resected lung adenocarcinomas to search for the incidence of p53 mutations and for record data on survival in each histological subtype, according to the new WHO criteria (1999). The frequency of p53 mutation in bronchioloalveolar carcinoma (BAC; 0% in 17 cases) and BAC with invasive growth component (BAC-invasive; 11% in 27 cases), which is conventionally categorized as the mixed subtype in WHO typing, were apparently significantly lower than in other types (non-BAC including acinar, papillary, solid, or mixed histology with these subtypes; 48% in 101 cases; P < 0.01). Multivariate analysis revealed that the histological subtype including BAC-invasive was a strong, independent, and significant prognostic factor (P < 0.03), as were tumor size and pathological stage (P < 0.001 and 0.002, respectively) for overall survival. However, the occurrence of p53 mutation itself was seen to be significant only in case of the univariate analysis. Therefore, histological subtyping may be a better prognostic indicator than is p53 mutation. These findings suggest that the WHO classification with the BAC and BAC-invasive from other histological subtypes may prove useful to predict the outcome for surgically treated patients with lung adenocarcinoma.

Adenocarcinoma↗
PubMed2001

[A case of pulmonary capillary hemangiomatosis].

In March 1995, a 54-year-old woman was admitted to a hospital because of exertional dyspnea and her condition was diagnosed as primary pulmonary hypertension. In September 1996, respiratory difficulty and hemosputum were woted. The chest computed tomographic scan showed diffuse micronodular opacities, and she was admitted to our hospital for examination of other pulmonary conditions giving rise to pulmonary hypertention. However no lung biopsy could be performed, because the pulmonary arterial pressure was too high. Although the patient received medication, she died of progressive right heart failure. The pathological diagnosis at autopsy was pulmonary capillary hemangiomatosis (PCH). Although PCH is a very rare disease that causes secondary pulmonary hypertension, it is important to distinguish it from primary pulmonary hypertension and pulmonary veno-occlusive disease.

Diagnosis, Differential↗
PubMed2000

Sp1 decoy transfected to carcinoma cells suppresses the expression of vascular endothelial growth factor, transforming growth factor beta1, and tissue factor and also cell growth and invasion activities.

Vasculature development is thought to be an important aspect in the growth and metastasis of solid tumors. Among the angiogenic factors produced by tumor cells, vascular endothelial growth factor is considered to be the most potent and pathologically important. The synthesis of this growth factor has been shown to be modulated through Sp1 function following stimulation by tumor necrosis factor alpha (TNF-alpha). Oligodeoxynucleotides (ODNs) were synthesized with either the consensus sequence for Sp1 binding (Sp1 decoy ODNs) or a mutated form of this sequence (mt-Sp1 decoy ODNs). Using the hemagglutinating virus of Japan (HVJ)-liposome method, we transferred these ODNs into cultured cancer cells (A549 and U251 cells). The TNF-alpha-mediated expression of both VEGF and transforming growth factor beta1 and tissue factor (TF) by the cancer cells could be simultaneously suppressed to less than 30% by transfection of Sp1 decoy ODNs but not by mt-Sp1 decoy ODNs. In addition, in vitro invasiveness, synthesis of mRNA for urokinase-type plasminogen activator, and cell proliferation of both cell lines were also inhibited to 40% by the transfection of only Sp1 decoy ODNs. These results suggested that the Sp1 decoy strategy would be effective for regulating tumor growth by simultaneously reducing cancer cell (a) angiogenic growth factor expression, (b) proliferation, and (c) invasiveness.

Adenocarcinoma↗
PubMed2000

Mixed chimerism, heart, and skin allograft tolerance in cyclophosphamide-induced tolerance.

We elucidated the possible role of chimerism in skin and heart allograft tolerance using cyclophosphamide (CP)-induced tolerance. When C3H (H-2k; Thy1.2, Mls-1b) mice were i.v. primed with 1x10(8) spleen cells (SC) from H-2 matched AKR (H-2k; Thy1.1, Mls-1a) mice and then treated i.p. with 200 mg/kg of CP, the survivals of both AKR skin grafts and heart grafts (HG) were permanently prolonged in a tolerogen-specific fashion. After this treatment, a minimal degree of mixed chimerism, the clonal destruction of Mls-1a-reactive CD4+Vbeta6+ T cells in the periphery, and the clonal deletion of Vbeta6+ thymocytes were all observed. When AKR SC and 100 mg/kg CP were used for conditioning, the AKR HG were permanently accepted, but the survival of the AKR skin grafts was only mildly prolonged. The clonal destruction of CD4+Vbeta6+ T cells in the periphery and the intrathymic clonal deletion of Vbeta6+ thymocytes were induced in both the SC and the 100 mg/kg CP-treated C3H mice. A minimal degree of mixed chimerism was detectable at 4 and 12 weeks after AKR SC and 100 mg/kg CP treatment, and still did not disappear at 40 weeks. The degree of mixed chimerism induced with SC and 100 mg/kg CP was significantly lower than that with SC and 200 mg/kg CP during the observation. No posttransplant cardiac allograft vasculopathy (CAV) was observed to develop, while both the Th1 type (interferon-gamma) and Th2 type (interleukin-4 and -10) cytokine expressions decreased in the AKR HG of the tolerant C3H mice treated with both AKR SC plus 200 mg/kg CP, and AKR SC plus 100 mg/kg CP. A second set of skin grafts from donor AKR mice survived for more than 100 days in a tolerogen-specific fashion in all C3H mice treated with AKR SC and 200 mg/kg CP and also accepted the AKR HG for over 200 days, while 80% of the C3H mice treated with AKR SC and 100 mg/kg CP and accepted the AKR HG for more than 200 days. These results strongly suggested the following conclusions: 1) the degree of chimerism can strongly influence the induction of skin and heart allograft tolerance, 2) posttransplant CAV does not develop in the donor HG maintained by chimerism-based CP-induced tolerance, 3) the mRNA expression of both Th1 and Th2 type cytokine decreased in the donor HG maintained by chimerism-based CP-induced tolerance, and 4) the induction of skin allograft tolerance is more difficult than the prevention of posttransplant CAV.

Animals↗
PubMed2000

Increased activity of nuclear factor-kappaB participates in cardiovascular remodeling induced by chronic inhibition of nitric oxide synthesis in rats.

BACKGROUND: Chronic inhibition of endothelial nitric oxide (NO) synthesis by the administration of N(omega)-nitro-L-arginine methyl ester (L-NAME) to rats induces early vascular inflammatory changes [monocyte infiltration into coronary vessels, nuclear factor-kappaB (NF-kappaB) activation, and monocyte chemoattractant protein-1 expression] as well as subsequent arteriosclerosis (medial thickening and perivascular fibrosis) and cardiac fibrosis. However, no direct evidence for the importance of NF-kappaB in this process is known. METHODS AND RESULTS: We examined the effect of a cis element decoy strategy to address the functional importance of NF-kappaB in the pathogenesis of cardiovascular remodeling. We found here that in vivo transfection of cis element decoy oligodeoxynucleotides against NF-kappaB to hearts prevented the L-NAME-induced early inflammation and subsequent coronary vascular medial thickening. In contrast, NF-kappaB decoy oligodeoxynucleotide transfection did not decrease the development of fibrosis, the expression of transforming growth factor-beta(1) mRNA, or systolic pressure overload induced by L-NAME administration. CONCLUSIONS: The NF-kappaB system participates importantly in the development of early vascular inflammation and subsequent medial thickening but not in fibrogenesis in this model. The present study may provide a new aspect of how endothelium-derived NO contributes to anti-inflammatory and/or antiarteriosclerotic properties of the vascular endothelium in vivo.

Animals↗
PubMed2000

The effects of caffeine on ATP-sensitive K(+) channels in smooth muscle cells from pig urethra.

The effects of caffeine on both levcromakalim-induced macroscopic and unitary currents in pig proximal urethra were investigated by the use of patch-clamp techniques (conventional whole-cell configuration and cell-attached configuration). The effects of caffeine were also examined on currents in inside-out patches of COS7 cells expressing carboxy terminus truncated inwardly rectifying K(+) channel (Kir6.2) subunits (i.e. Kir6.2DeltaC36) which form ATP-sensitive K(+) channels (K(ATP) channels). In conventional whole-cell configuration, the levcromakalim (100 microM)-induced inward current (symmetrical 140 mM K(+) conditions) was inhibited by caffeine (> or =1 mM) at a holding potential of -50 mV. In contrast, ryanodine (10 microM) caused no significant inhibitory effect on the gradual decay of the levcromakalim-induced current at -50 mV. The amplitude of the 30 microM levcromakalim-induced current was enhanced by 3-isobutyl-1-methylxanthine (IBMX, 100 microM). In cell-attached configuration, the levcromakalim-induced K(+) channel openings were inhibited by subsequent application of 10 mM caffeine, decreasing the channel open probability at -50 mV. Reverse transcriptase-polymerase chain reaction (RT - PCR) analysis revealed the presence of Kir6.2 transcript in pig urethra. Caffeine (> or =3 mM) inhibited the channel activity of Kir6.2DeltaC36 expressed in COS7 cells (3 mM caffeine, 65+/-6%, n=4; 10 mM caffeine, 29+/-2%, n=4). These results suggest that caffeine can inhibit the activity of K(ATP) channels through a direct blocking effect on the pore-forming Kir subunit.

1-Methyl-3-isobutylxanthine↗
PubMed2000

Moyamoya disease.

Moyamoya disease is a specific chronic cerebrovascular occlusive disease first reported by Japanese surgeons in 1957. The disease is characterized by stenosis or occlusion of the terminal portions of the bilateral internal carotid arteries and abnormal vascular network in the vicinity of the arterial occlusion. It may cause ischemic attacks or cerebral infarction, which is more frequent in children than in adults. In adults, cerebral hemorrhage may occur. The disease is distributed in all age groups, but the highest peak is in childhood at less than 10 years of age. The characteristic histopathologic features of the steno-occlusive arteries are fibrocellular thickening of the intima containing proliferated smooth muscle cells and prominently tortuous and often duplicated internal elastic lamina. There is usually no atheromatous plaque in the arterial wall. Etiology of the disease is still unknown; however, multifactorial inheritance is considered possible because of a higher incidence of the disease in Japanese and Koreans and approximately 10% of familial occurrence among the Japanese. Recent genetic studies suggest some responsible genetic foci in chromosomes 3, 6 and 17.

Carotid Artery, Internal↗
PubMed2000

Angiogenesis and its regulation: roles of vascular endothelial cell growth factor.

Neovascularization is well known to occur in human atherosclerotic plaques, proliferative retinopathies, and malignant neoplasias. However, its pathophysiologic roles and mechanisms still remain unclear. In this study, histochemical examination of atherosclerotic plaques showed that vascular endothelial cell growth factor (VEGF) was expressed by the smooth muscle cells and foamy macrophages in the atherosclerotic intimas. The number of VEGF-positive cells was positively correlated with the number of intimal blood vessels. Moreover, VEGF gene transfer into rabbit carotid arteries using the hemagglutinating virus of Japan (HVJ)-liposomes showed that VEGF overexpression could induce the angiomatoid proliferation. In diabetic rats, VEGF was overexpressed in diabetic retinas, and thus the local overexpression of VEGF seemed to play an important role in the development of blood-retinal barrier breakdown in simple diabetic retinopathy. These results indicated that the VEGF can act as a local and endogenous regulator of endothelial cell functions and that VEGF induces the neovascularization under pathophysiologic conditions. On the other hand, the transfer of a decoy for the cis-element in the promoter region of the angiogenic factors would be an effective method for regulating angiogenesis, because other angiogenic factors' expression promoted by such cis-element could be simultaneously suppressed. Therefore, this method may supply a useful therapeutic tool for the regulation of pathologic angiogenesis.

Animals↗
PubMed2000

Lung development following diaphragmatic hernia in the fetal rabbit.

Diaphragmatic hernia was created in 39 rabbit fetuses on day 23 of gestation. Fifteen fetuses underwent a sham thoracotomy (SHAM). Thirty-nine non-operated littermates served as internal controls (CTR). Fetuses were harvested by Caesarean section on days 25, 27, 29 and 30 of gestation. Pulmonary response was evaluated by lung to body weight ratio (LBWR), morphometry, and density of type II pneumocytes. No difference was found between CTR and SHAM fetuses at term. CDH fetuses had smaller lungs (LBWR 0.014 +/- 0.004 versus 0.030 +/- 0.04 in CTR, P < 0.0001), a less complex acinus [mean terminal bronchial density (MTBD) 1.786 +/- 0.408 versus 0.917 +/- 0. 188, P < 0.0001], thicker alveolar septa [mean wall transection length (LMW) 0.0221 +/- 0.008 versus 0.0142 +/- 0.002, P = 0.0003], and a lower type II cell count (144.5 +/- 19.33 versus 216.2 +/- 27.85 per high power field, P < 0.0001). The differences in MTBD and LMW were significant from gestational day 25 onwards, and the differences in type II cell count from day 27 onwards. Surgical diaphragmatic hernia in rabbit fetuses in the late pseudoglandular phase reproduces many features of the pulmonary hypoplasia associated with human congenital diaphragmatic hernia, including the delayed maturation. The effects are present within 2 days following experimental diaphragmatic hernia and progress over time.

Animals↗
PubMed2000

Anti-monocyte chemoattractant protein-1 gene therapy inhibits vascular remodeling in rats: blockade of MCP-1 activity after intramuscular transfer of a mutant gene inhibits vascular remodeling induced by chronic blockade of NO synthesis.

Monocyte chemoattractant protein-1 (MCP-1) may play an essential part in the formation of arteriosclerosis by recruiting monocytes into the arterial wall. Thus, we devised a new strategy for anti-MCP-1 gene therapy against arteriosclerosis by transfecting an amino-terminal deletion mutant (missing the amino-terminal amino acids 2 to 8) of the human MCP-1 gene into a remote organ (skeletal muscles). Intramuscular transduction with the mutant MCP-1 gene blocked monocyte recruitment induced by a subcutaneous injection of recombinant MCP-1. In a rat model in which the chronic inhibition of endothelial nitric oxide synthesis induces early vascular inflammation as well as subsequent coronary vascular remodeling, this strategy suppressed monocyte recruitment into the coronary vessels and the development of vascular medial thickening, but did not reduce perivascular fibrosis. Thus, MCP-1 is necessary for the development of medial thickening but not for fibrosis in this model. This new strategy may be a useful and feasible gene therapy against arteriosclerosis.

Animals↗
PubMed1999

Target gene transfer of tissue plasminogen activator to cornea by electric pulse inhibits intracameral fibrin formation and corneal cloudiness.

Intracameral fibrin formation, a complication of ocular inflammation and intraocular operations, sometimes results in glaucoma and/or corneal damage leading to permanent visual loss. We transferred a therapeutic gene to the corneal endothelium in order to use it as a therapeutic organ. A plasmid encoding tissue plasminogen activator (tPA) was injected into the anterior chamber of rats and electric pulses (EPs) were given subsequently, which transferred a plasmid gene to a highly selected area of corneal endothelium with no inflammation. The biologically active tPA was clearly present for 4 days after treatment. Fibrin formation induced by YAG laser-generated bleeding in the anterior chamber decreased significantly more in treated eyes than in control eyes. Corneal opacity was significantly lower in treated eyes than in control eyes and histological damage was not apparent in the treated eyes. This genetic modification allows us to use the corneal endothelium to treat various ocular diseases and could be a new and effective type of pharmacologic gene therapy.

Animals↗
PubMed1999

A clinicopathologic study of transient osteoporosis of the hip.

OBJECTIVE: It has been proposed that transient osteoporosis of the hip (TOH) may represent the early reversible phase of osteonecrosis of the femoral head (ON). The purpose of this study was to investigate the clinicopathologic characteristics of three cases of TOH. DESIGN AND PATIENTS: A bone biopsy was performed on three patients who had been diagnosed as having TOH based on the clinical course, radiograph, bone scintigram, and MR images. The biopsy specimens were studied histopathologically by light and electron microscopy. RESULTS: The most characteristic feature of TOH was focal areas of thin and disconnected bone trabeculae covered by osteoid seams and active osteoblasts. The surrounding bone marrow tissue showed edematous changes and mild fibrosis, frequently associated with vascular congestion and/or interstitial hemorrhage. No osteonecrotic region was observed in either the bone trabeculae or the bone marrow tissue. All patients have improved clinically and in the 3.5-9 years of follow-up have shown no evidence of ON. CONCLUSIONS: This study supports the concept that transient osteoporosis of the hip is a distinct entity.

Adult↗
PubMed1999

Bile ductular proliferation as a prognostic factor in biliary atresia: an immunohistochemical assessment.

PURPOSE: The correlation between the histological findings of the intrahepatic biliary epithelium and postoperative bile drainage in biliary atresia (BA) was investigated. METHODS: The patients with BA were classified into 2 groups, consisting of a good bile drainage group (GBD, n = 14, mean age at initial operation, 57.6+/-18.0 days) and a poor bile drainage group (PBD, n = 11, mean age at initial operation, 86.9+/-42.7 days). Liver specimens from an initial Kasai's operation were examined by immunostaining using anticytokeratin 7 (CK7) antibody and anti-MIB-1 antibody. The number of CK7-positive cells in the bile ductules was microscopically calculated within the 40-microm-thick interstitium along the limiting plate (LP), and the CK7-positive cell number per unit length of the LP was estimated. In addition, the MIB-1 index in bile ductules also was determined. RESULTS: The number of CK7-positive cells in PBD was significantly higher than that in GBD (167.6+/-45.6 v 117.8+/-32.4/ mm, P<.05). However, the MIB-1 index in biliary cells did not differ between the 2 groups. CONCLUSION: An increased number of intrahepatic bile duct epithelial cells in liver specimens at the initial operation may be a poor prognostic factor in BA and appears to depend on the duration of bile stasis rather than the degree of bile stasis.

Analysis of Variance↗
PubMed1999

Monkey hepatocytes efficiently express tissue factor pathway inhibitor (TFPI), in contrast with human and rat hepatocytes.

It has been reported that tissue factor pathway inhibitor (TFPI), a Kunitz-type protease inhibitor that regulates the extrinsic blood coagulation pathway, is not expressed in human, bovine, rabbit, or rat liver. Here, we found that TFPI is efficiently expressed in Macaque monkey liver. Monkey hepatocytes were identified as the expression cells by Northern blot analysis. The hepatocytes were stained with anti-human TFPI antibody, as were endothelial cells of the small vessels. We isolated and sequenced the 5'-flanking 1.4 kb regions of monkey and human TFPI genes, and found them to show 92.6% identity in their nucleotide sequences. We measured their transcriptional activities using a luciferase reporter gene and showed that the activity of the monkey TFPI gene is higher than that of the human gene in monkey primary hepatocytes. Although the binding motif of hepatocyte nuclear factor-1 is present only in the monkey gene, the site does not seem to be involved in the transcriptional activity. Mutagenetic analyses revealed that the region from -138 to +28 in the monkey gene is important for the expression of TFPI in hepatocytes. The present study indicates that the expression of the monkey TFPI gene is regulated by different mechanisms from the human TFPI gene.

Animals↗
PubMed1999

Immunohistochemical expression of vascular endothelial growth factor/vascular permeability factor in atherosclerotic intimas of human coronary arteries.

Neovascularization is well known to occur in human atherosclerotic plaques; however, its pathophysiological roles, mechanisms, and stimuli in atherogenesis still remain unclear. In this study, 525 tissue blocks of coronary artery tissue obtained at autopsy from 48 patients ranging in age from 20 to 93 years old (mean+/-SD, 71+/-15 years) were immunohistochemically examined for vascular endothelial growth factor (VEGF) expression in the atherosclerotic intimas. The atherosclerotic lesions were histopathologically classified into types I through VI, as proposed by the American Heart Association Committee, and the numbers of intimal blood vessels and VEGF-positive cells were then morphometrically counted in sections that were immunohistochemically examined with anti-CD34 and human VEGF antibodies, respectively. The more the atherosclerotic lesion type advanced, the more often the lesion contained intimal blood vessels, which were expressed as percentages of the intimal section with intimal microvessels, viz, diffuse intimal thickening (DIT): 0% (0/111); type I, 31% (32/104); II, 42% (10/24); III, 66% (77/117); IV, 72% (48/67); V, 79% (70/89); and VI, 100% (13/13), P<0.0001. The number of VEGF-positive cells per intimal section was also positively correlated with the number of intimal blood vessels (P<0. 0001). The VEGF-positive cells were scattered in the fibrous caps as well as the shoulders and deeper areas of the plaques, and the double-immunostaining method revealed that the VEGF-positive cells were largely spindle-shaped, smooth muscle cells with some macrophage-derived foam cells. These findings thus suggest the possibility that the VEGF expressed by the smooth muscle cells and foamy macrophages in the atherosclerotic intimas can act as a local and endogenous regulator of endothelial cell functions, including intimal neovascularization, in atherosclerotic lesions of human coronary arteries.

Adult↗
PubMed1999

Prevalence of intracranial saccular aneurysms in a Japanese community based on a consecutive autopsy series during a 30-year observation period. The Hisayama study.

BACKGROUND AND PURPOSE: Subarachnoid hemorrhage is a life-threatening disease that occurs mostly because of the rupture of intracranial saccular aneurysms. However, little is known about the prevalence of ruptured and unruptured aneurysms in the general population. The aim of the present study was to examine the prevalence of intracranial aneurysms on the basis of a consecutive autopsy series over a 30-year observation period in a general Japanese population in Hisayama. METHODS: We evaluated 1230 consecutive autopsy cases with craniotomy among the total deaths of Hisayama residents during 1962 through 1991 (overall autopsy rate, 80.1%). RESULTS: A total of 73 intracranial saccular aneurysms were found in 57 cases (4.6%). The prevalence of aneurysms for women was 2.4 times higher than that for men (7.1% versus 2.9%). Among men, the prevalence of aneurysms remained unchanged across the range of age groups. In contrast, there were 2 peaks in the prevalence of aneurysms for women falling in the 40- to 49-year (14.3%) and 60- to 69-year age groups (14.5%). The most common site of the aneurysms was the middle cerebral artery (31.5%), followed by the anterior communicating artery (30.1%), anterior cerebral artery (15.1%), vertebrobasilar artery (12.3%), and internal carotid artery (11.0%). Among these 73 aneurysms, 29 (39.7%) were ruptured. Ruptured aneurysms were common in subjects <80 years of age, whereas unruptured aneurysms were prevalent in those >/=80 years of age. The frequency of ruptured aneurysms was highest in the vertebrobasilar system (66.7%) and lowest in the middle cerebral artery (13.0%). CONCLUSIONS: Our data suggest that intracranial aneurysms are more frequent in women in the general Japanese population. Aneurysms are more prevalent in the middle cerebral artery, but the risk of rupture is highest in the vertebrobasilar system.

Adolescent↗
PubMed1998

Transfer of wild-type p53 gene effectively inhibits vascular smooth muscle cell proliferation in vitro and in vivo.

Wild-type p53 (wt-p53), a key protein in cell cycle regulation, inactivates the G1 cyclins through direct activation of p21Waf-1/Cip-1/Sdi-1. Persistent vascular smooth muscle cell (VSMC) proliferation following vascular interventions hinders the benefits of these therapeutics. Using the hemagglutinating virus of Japan/liposome-mediated gene transfer method, we examined the inhibitory effect of overexpression of exogenous wt-p53 on VSMC proliferation in vitro and in vivo. We assessed the proliferative activity of human p53 cDNA-transduced bovine VSMCs by DNA synthesis assay, flow cytometry, and cell proliferation assay. p53 gene transfer reduced thymidine incorporation of VSMCs stimulated by platelet-derived growth factor-BB (P<.001). The p53-transduced VSMCs underwent synthetic phase depletion (mean, 8.02% versus 33.7% of control; P<.001) and transient G2/M accumulation 2 days after gene transfection, and in almost all cells, G1 arrest occurred (mean, 92.6% versus 79.3% of control; P<.001) 5 days later. The wt-p53 gene transfection also inhibited the VSMC proliferation (P<.001) with no detectable induction of apoptosis. Cell death of p53-transduced VSMCs was induced only by additional treatment with an apoptosis-stimulating reagent, doxorubicin. The verification of apoptosis was made by DNA ladder, flow cytometry, and electron microscopy. In vivo transfection of p53 cDNA inhibited neointimal formation after balloon injury in rabbit carotid arteries, without apoptotic stimuli (P<.01). Thus, overexpression of the p53 gene in the injured arterial wall inhibits the proliferation of VSMCs in vitro and in vivo. This novel concept, including not only exogenous but also endogenous p53 overexpression in the vessel wall, may be one approach worth exploring in the treatment of patients with restenosis occurring after vascular interventions.

Animals↗