Magnetite (Fe3O4) nanocrystals affect the expression of genes involved in the TGF-beta signalling pathway

2011 ◽  
Vol 7 (5) ◽  
pp. 1481 ◽  
Author(s):  
Jameel Ahmad Khan ◽  
Tarun Kumar Mandal ◽  
Taposh Kumar Das ◽  
Yogendra Singh ◽  
Beena Pillai ◽  
...  
2019 ◽  
Vol 52 (4) ◽  
Author(s):  
Hongke Luo ◽  
Yuchen Guo ◽  
Yuting Liu ◽  
Yuan Wang ◽  
Rixin Zheng ◽  
...  

Development ◽  
1998 ◽  
Vol 125 (15) ◽  
pp. 2803-2811 ◽  
Author(s):  
Z. Hardcastle ◽  
R. Mo ◽  
C.C. Hui ◽  
P.T. Sharpe

The expression of genes involved in the Sonic Hedgehog signalling pathway, including Shh, Ptc, Smo, Gli1, Gli2 and Gli3, were found to be expressed in temporal and spatial patterns during early murine tooth development, suggestive of a role in early tooth germ initiation and subsequent epithelial-mesenchymal interactions. Of these Ptc, Smo, Gli1, Gli2 and Gli3 were expressed in epithelium and mesenchyme whereas Shh was only detected in epithelium. This suggests that Shh is involved in both lateral (epithelial-mesenchymal) and planar (epithelial-epithelial) signalling in early tooth development. Ectopic application of Shh protein to mandibular mesenchyme induced the expression of Ptc and Gli1. Addition of exogenous Shh protein directly into early tooth germs and adjacent to tooth germs, resulted in abnormal epithelial invagination, indicative of a role for Shh in epithelial cell proliferation. In order to assess the possible role of this pathway, tooth development in Gli2 and Gli3 mutant embryos was investigated. Gli2 mutants were found to have abnormal development of maxillary incisors, probably resulting from a mild holoprosencephaly, whereas Gli3 mutants had no major tooth abnormalities. Gli2/Gli3 double homozygous mutants did not develop any normal teeth and did not survive beyond embryonic day 14.5; however, Gli2(−/−); Gli3(+/−) did survive until birth and had small molars and mandibular incisors whereas maxillary incisor development was arrested as a rudimentary epithelial thickening. These results show an essential role for Shh signalling in tooth development that involves functional redundancy of downstream Gli genes.


1995 ◽  
Vol 269 (2) ◽  
pp. H638-H647 ◽  
Author(s):  
M. O. Boluyt ◽  
X. Long ◽  
T. Eschenhagen ◽  
U. Mende ◽  
W. Schmitz ◽  
...  

Chronic infusion of isoproterenol (Iso) in rats results in cardiac hypertrophy via incompletely understood mechanisms. Our purpose was to determine whether Iso infusion would alter the expression of genes associated with hypertrophy. Male Wistar rats received either 2.4 mg Iso.kg-1.day-1, 9.9 mg propranolol (Prop).kg-1.day-1, both Iso and Prop, or vehicle (NaCl) via subcutaneously implanted osmotic pumps. In Iso-treated rats, the ventricular weight-to-body weight ratio was increased by 27% after 1 day and peaked on day 3 (+ 40%). Levels of atrial natriuretic factor (ANF) and fibronectin (FN) mRNA in the left ventricles were elevated 20-fold and 13-fold in Iso-treated rats, respectively, peaking at 3 days of infusion. The increase in FN mRNA accumulation was at least partially accounted for by elevated expression of extra type IIIA and IIIB (EIIIA and EIIIB) splicing variants. Levels of transforming growth factor (TGF)-beta 1 mRNA were elevated twofold after 3 days of Iso infusion. The abundance of skeletal alpha-actin (SK) mRNA increased fourfold after 1 day of Iso and declined thereafter. Iso infusion decreased sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) and preproenkephalin (PNK) gene expression by approximately 50% and induced a myosin heavy chain (MHC) isogene switch favoring beta-MHC. Prop partially inhibited the Iso-evoked increases in ANF and FN mRNA, completely prevented the Iso-induced changes in TGF-beta 1 and SERCA mRNA, but had no effect on the Iso-stimulated changes in SK and PNK gene expression. These results demonstrate that chronic Iso infusion elicits alterations in cardiac gene expression that are consistent with the development of myocyte hypertrophy and interstitial fibrosis and are directionally identical to those previously reported for pressure overload hypertrophy.


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