Interstitial dendritic cells of the rat heart. Quantitative and ultrastructural changes in experimental myocardial infarction.

Zhang, Jun; Yu, Zu‐Xi; Fujita, Shinsuke; Yamaguchi, Maria; Ferrans, Víctor J.

doi:10.1161/01.cir.87.3.909

Cited by 65 publications

(74 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These investigators suggested the presence of DC by immunohistochemical staining using OX6 Ab (30). However, OX6 Ab recognizes the MHC class II molecule, which is expressed on several types of APCs as well as DC.…”

Section: Discussionmentioning

confidence: 99%

Differential Effects of GM-CSF and G-CSF on Infiltration of Dendritic Cells during Early Left Ventricular Remodeling after Myocardial Infarction

Naito

Anzai

Sugano

et al. 2008

The Journal of Immunology

View full text Add to dashboard Cite

Several lines of evidence suggest that the immune activation after myocardial infarction (MI) induces secondary myocardial injury. Although dendritic cells (DC) are potent regulators of immunity, their role in MI is still undetermined. We investigated the effect of DC modulation by CSF on left ventricular (LV) remodeling after MI. MI was induced by ligation of the left coronary artery in male Wistar rats. G-CSF (20 μg/kg/day, MI-G, n = 33), a GM-CSF inducer (romurtide, 200 μg/kg/day, MI-GM, n = 28), or saline (MI-C, n = 55) was administered for 7 days. On day 14, MI-G animals had higher LV max dP/dt and smaller LV dimensions, whereas MI-GM animals had lower LV max dP/dt and larger LV dimensions than did MI-C animals, despite similar infarct size. In MI-C, OX62+ DC infiltrated the infarcted and border areas, peaking on day 7. Bromodeoxyuridine-positive DC were observed in the border area during convalescence. Infiltration by DC was decreased in MI-G animals and increased in MI-GM animals compared with MI-C (p < 0.05). In the infarcted area, the heat shock protein 70, TLR2 and TLR4, and IFN-γ expression were reduced in MI-G, but increased in MI-GM in comparison with those in MI-C animals. IL-10 expression was higher in MI-G and lower in MI-GM than in MI-C animals. In conclusion, G-CSF improves and GM-CSF exacerbates early postinfarction LV remodeling in association with modulation of DC infiltration. Suppression of DC-mediated immunity could be a new strategy for the treatment of LV remodeling after MI.

show abstract

Section: Discussionmentioning

confidence: 99%

Differential Effects of GM-CSF and G-CSF on Infiltration of Dendritic Cells during Early Left Ventricular Remodeling after Myocardial Infarction

Naito

Anzai

Sugano

et al. 2008

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…7,12,35 OX6 is an antibody against rat major histocompatibility complex (MHC) class II antigen (Ia) that is mainly expressed on activated macrophages, dendritic cells, and B cells. 35,49,50 ␣-SMA has been recognized to be induced in developing myofibroblastic cells in fibrotic lesions, and anti-␣-SMA antibody has been used to detect the cells. 2,11,15,26,27,33,43,45 Terminal deoxyribonucleotide transferase (TdT)-mediated deoxyuridine triphosphate nick end labeling (TUNEL) for apoptotic cells A standard in situ TUNEL (Apop Tag Kit, Oncor Inc., Gaithersburg, MD) method was used for detection of DNA fragmentation in apoptotic cells.…”

Section: Histopathology and Immunohistochemistrymentioning

confidence: 99%

Participation of Different Macrophage Populations and Myofibroblastic Cells in Chronically Developed Renal Interstitial Fibrosis after Cisplatin-induced Renal Injury in Rats

et al. 2002

View full text Add to dashboard Cite

Abstract. To shed some light on the mechanisms behind renal fibrogenesis, the present study immunohistochemically investigated the participation of different macrophage populations and myofibroblastic cells in rat renal interstitial fibrosis developed chronically after repeated injection of cisplatin (2 mg/kg body weight, once weekly for 7 weeks). During the 19-week recovery period after the final injection, fibrotic lesions progressively developed in the corticomedullary junction, with the greatest level at post-final injection (FPI) week 5, and then the lesions were gradually repaired by PFI week 19, indicative of a healing process. In conformity with the development of fibrotic lesions, the number of myofibroblastic cells reacting with an anti-␣-smooth muscle actin antibody was increased, with a peak at PFI week 3, and collagens (types I, III, and IV), fibronection, and laminin were excessively accumulated in these areas. Interstitial cells forming the fibrotic lesions showed mitotic activity at the early stages, whereas they disappeared by apoptosis in the healing process. A large number of cells reacting with an antibody of ED1 (for exudate macrophages), ED2 (for resident macrophages), or OX6 (for major histocompatibility complex class II-presenting macrophages and interstitial dendritic cells) had already appeared at PF1 week 1, and then their numbers increased, with a peak at PFI weeks 7, 3, and 9 in ED1-, ED2-, and OX6-positive cells, respectively. Thereafter, the number of ED1-and ED2-positive cells decreased, whereas the number of OX6-positive cells persisted at a high level until PFI week 19. In the healing process, clusters of lymphocytes were present, the development of which might have been related to OX6-positive cells. The present study demonstrated that chronically developing rat renal interstitial fibrosis might be produced by the complicated mechanisms evoked by interactions between different macrophage populations and myofibroblastic cells, because macrophages show heterogeneous functions depending on microenvironmental factors.

show abstract

“…These cells have also been regarded as key cells in experimentally induced fibrosis of the liver (12,14,24,42), lungs (11,16,32,36,47), and heart (22,46). Macrophage-produced growth factors, transforming growth factor-(3 (TGF- (3) in particular, induce the conversion of pre-existing fibroblasts into myofibroblasts.…”

Section: Introductionmentioning

confidence: 99%

Immunohistochemical Analysis of Macrophages, Myofibroblasts, and Transforming Growth Factor-β Localization during Rat Renal Interstitial Fibrosis Following Long-Term Unilateral Ureteral Obstruction

et al. 1998

View full text Add to dashboard Cite

Renal interstitial fibrosis was induced in rats by chronic unilateral ureteral obstruction (UUO). To identify the mechanisms behind the fibrosis, macrophage influx, myofibroblast involvement, and the localization of transforming growth factor-β (TGF-β, a fibrogenic cytokine) were investigated immunohistochemically in rats euthanatized at 0 (controls), 3,6,9,12, and 15 days after UUO. The number of α-smooth muscle actin-positive myofibroblasts began to increase significantly in the medulla from day 3, and the development of medullary fibrosis was confirmed from day 6 by morphometric analysis. From day 9, papillary fibrosis also developed in association with an increased number of myofibroblasts. These myofibroblasts showed a parallel orientation to the mucosal surface of the pelvis. In the medulla and papilla, from day 6 the number of ED1 (primary antibody)-positive macrophages began to increase significantly. There appeared to be a relationship between macrophage influx and myofibroblast involvement. By contrast, in the cortex there was no marked increase in myofibroblasts nor development of fibrotic tissues, regardless of increased number of macrophages from day 6. Immunohistochemically, no staining for TGF-β was found in infiltrating macrophages or myofibroblasts. However, TGF-& b e t a ; was localized on some cortical proximal renal tubules both of normal control and obstructed kidneys in the early stages on days 3, 6, and 9, suggesting that the possible origin of TGF-β may be renal epithelia. However, the staining intensity for TGF-β on the renal epithelia tended to be weakened in advanced obstructed kidneys on days 12 and 15. The likely contribution of TGF-β to the advanced stages of UUO-induced renal fibrosis remains to be determined.

show abstract

Interstitial dendritic cells of the rat heart. Quantitative and ultrastructural changes in experimental myocardial infarction.

Cited by 65 publications

References 31 publications

Differential Effects of GM-CSF and G-CSF on Infiltration of Dendritic Cells during Early Left Ventricular Remodeling after Myocardial Infarction

Differential Effects of GM-CSF and G-CSF on Infiltration of Dendritic Cells during Early Left Ventricular Remodeling after Myocardial Infarction

Participation of Different Macrophage Populations and Myofibroblastic Cells in Chronically Developed Renal Interstitial Fibrosis after Cisplatin-induced Renal Injury in Rats

Immunohistochemical Analysis of Macrophages, Myofibroblasts, and Transforming Growth Factor-β Localization during Rat Renal Interstitial Fibrosis Following Long-Term Unilateral Ureteral Obstruction

Contact Info

Product

Resources

About