Omentum facilitates liver regeneration.
ABSTRACT To investigate the mechanism of liver regeneration induced by fusing the omentum to a small traumatic injury created in the liver. We studied three groups of rats. In one group the rats were omentectomized; in another group the omentum was left in situ and was not activated, and in the third group the omentum was activated by polydextran particles.
We pre-activated the omentum by injecting polydextran particles and then made a small wedge wound in the rat liver to allow the omentum to fuse to the wound. We monitored the regeneration of the liver by determining the ratio of liver weight/body weight, by histological evaluation (including immune staining for cytokeratin-19, an oval cell marker), and by testing for developmental gene activation using reverse transcription polymerase chain reaction (RT-PCR).
There was no liver regeneration in the omentectomized rats, nor was there significant regeneration when the omentum was not activated, even though in this instance the omentum had fused with the liver. In contrast, the liver in the rats with the activated omentum expanded to a size 50% greater than the original, and there was histologically an interlying tissue between the wounded liver and the activated omentum in which bile ducts, containing cytokeratin-19 positive oval cells, extended from the wound edge. In this interlying tissue, oval cells were abundant and appeared to proliferate to form new liver tissue. In rats pre-treated with drugs that inhibited hepatocyte growth, liver proliferation was ongoing, indicating that regeneration of the liver was the result of oval cell expansion.
Activated omentum facilitates liver regeneration following injury by a mechanism that depends largely on oval cell proliferation.
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ABSTRACT: Interstitial pulmonary fibrosis is caused by the excess production of extracellular matrix (ECM) by Fb in response to TGF-β1. Here, we show that the peptidyl-prolyl isomerase Pin1 modulates the production of many pro- and antifibrogenic cytokines and ECM. After acute, bleomycin injury, Pin1(-/-) mice showed reduced, pulmonary expression of collagens, tissue inhibitors of metalloproteinases, and fibrogenic cytokines but increased matrix metalloproteinases, compared with WT mice, despite similar levels of inflammation. In primary fibroblasts, Pin1 was required for TGF-β-induced phosphorylation, nuclear translocation, and transcriptional activity of Smad3. In Pin1(-/-) cells, inhibitory Smad6 was found in the cytoplasm rather than nucleus. Smad6 knockdown in Pin1(-/-) fibroblasts restored TGF-β-induced Smad3 activation, translocation, and target gene expression. Therefore, Pin1 is essential for normal Smad6 function and ECM production in response to injury or TGF-β and thus may be an attractive therapeutic target to prevent excess scarring in diverse lung diseases.Journal of Biological Chemistry 05/2012; 287(28):23294-305. · 4.65 Impact Factor
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ABSTRACT: Omental cells (OCs) are shown to help wound healing. The purpose of this study is to investigate if OCs improve cornea repair after alkali injury by subconjunctival injection of activated OCs in rats. Forty eight hours after limbal corneal alkali injury, fresh isolated OCs were injected subconjunctivally into the recipient rat’s eye. Prior to the injury and at 0, 4 and 8 days after injury, the eyes were examined using slit lamp biomicroscopy. Corneal opacification and corneal neovascularization were graded in a masked fashion. The inflammatory response to the injury was evaluated by counting neutrophil cell numbers in the cornea under microscope. There was no significant difference in corneal opacification between the control and OCs treatment groups; however, the corneal neovascularization was significantly less in the eyes treated with OCs as compared to the controls. Also OCs treatment markedly decreased neutrophil infiltration after corneal-limbal alkali injury. Our results suggest that OCs may have a beneficial role in corneal healing after limbal corneal alkali injury by suppressing inflammatory cell infiltrates and corneal neovascularization.Experimental Eye Research 01/2014; · 3.03 Impact Factor
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ABSTRACT: OBJECTIVES: Anastomotic leakage is a major cause of mortality in oesophageal surgery. Whether omentoplasty after oesophagogastrostomy could reduce anastomotic leakage is still controversial. The aim of this study is to investigate the function of omentoplasty to reinforce cervical oesophagogastrostomy after radical oesophagectomy with three-field lymphadenectomy. METHODS: A total of 184 patients who underwent radical oesophagectomy with three-field lymphadenectomy took part in this prospective study. Patients were randomized to receive either the omentoplasty or non-omentoplasty. In the omentoplasty group, the omentum was wrapped around the oesophagogastric anastomosis after oesophagogastrostomy. Age, gender, location of carcinoma, stage, body mass index, diabetes, coronary artery disease, peripheral vascular disease and performance of omentoplasty were recorded. The anastomotic leakage and stricture and recurrence site were followed up for three years after the operation. RESULTS: The two groups were comparable in terms of age, gender, location of carcinoma, stage, body mass index, diabetes, coronary artery disease and peripheral vascular disease (P > 0.05). In contrast to the non-omentoplasty group with a postoperative anastomotic leakage rate of 9.8%, the omentoplasty subjects demonstrated a significantly lower rate of 3.3% (P < 0.05). No lethal leakage was found in the omentoplasty group, while two non-omentoplasty patients developed incurable empyema and mediastinitis due to leakage and ultimately died. The rate of incidence of anastomotic stricture in the omentoplasty and non-omentoplasty groups were 4.3% and 2.2% respectively. Of the five cases of death during the hospital stay, two were found in the omentoplasty group and three in non-omentoplasty. There was no significant difference of lethal leakage, stricture and death rate between the two groups (P > 0.05). The hospital stay was significantly longer for non-omentoplasty patients, compared with that for the omentoplasty subjects (P < 0.05). Tumour recurrence in lymphatic- or haematogenous metastasis was similar in both groups (P > 0.05). CONCLUSION: Omentoplasty may prevent anastomotic leakage of oesophagogastrostomy following radical oesophagectomy with three-field lymphadenectomy.European journal of cardio-thoracic surgery: official journal of the European Association for Cardio-thoracic Surgery 05/2012; · 2.40 Impact Factor