Liver Disease Stem Cell Treatment

Liver Disease and Stem Cell Therapy at SIRM

 

Liver Disease and Stem Cell Treatment

Liver Disease and Stem Cell Treatment

What is Liver Disease?
The liver is under your ribs on the right hand side. The liver is the largest organ in the body and if the liver fails completely then untreated only 3-4 days to find a donor liver for a possible transplant.

Corrently there is no such thing as an artificial liver.

The liver not only produces many proteins it creates energy from our food. The liver removes waste products in our body and also removes unwanted drugs such as nicotine and alcohol.

The most common Liver conditions include infections such as hepatitis A, B, C, E, alcohol damage, fatty liver, cirrhosis, cancer, drug damage especially paracetamol (acetaminophen) and cancer drugs.

 

The liver does not have any pain nerves so liver disease can be unexpected.
Liver disease is commonly related to alcohol and diet problems.

 


STEM CELL RESEARCH



Use of hepatocyte and stem cells for treatment of post-resectional liver failure: are we there yet?

Ezzat TM, Dhar DK, Newsome PN, Malagó M, Olde Damink SW.


2011 Jul;31(6):773-84. doi: 10.1111/j.1478-3231.2011.02530.x. Epub 2011 Apr 19.

Source
HPB and Liver Transplantation Surgery, Royal Free Hospital, University College London, Pond Street, London, UK.


Abstract
Post-operative liver failure following extensive resections for liver tumours is a rare but significant complication. The only effective treatment is liver transplantation (LT); however, there is a debate about its use given the high mortality compared with the outcomes of LT for chronic liver diseases.

Cell therapy has emerged as a possible alternative to LT especially as endogenous hepatocyte proliferation is likely inhibited in the setting of prior chemo/radiotherapy. Both hepatocyte and stem cell transplantations have shown promising results in the experimental setting; however, there are few reports on their clinical application.

This review identifies the potential stem cell sources in the body, and highlights the triggering factors that lead to their mobilization and integration in liver regeneration following major liver resections.

Therapeutic plasticity of stem cells and allograft tolerance.

Cytotherapy. 2011 May 10;

Authors: Sordi V, Piemonti L

Abstract Transplantation is the treatment of choice for many diseases that result in organ failure, but its success is limited by organ rejection. Stem cell therapy has emerged in the last years as a promising strategy for the induction of tolerance after organ transplantation. Here we discuss the ability of different stem cell types, in particular mesenchymal stromal cells, neuronal stem/progenitor cells, hematopoietic stem cells and embryonic stem cells, to modulate the immune response and induce peripheral or central tolerance.

These stem cells have been studied to explore tolerance induction to several transplanted organs, such as heart, liver and kidney. Different strategies, including approaches to generating tolerance in islet transplantation, are discussed here.

PMID: 21554176 [PubMed - as supplied by publisher]

 

 

Impaired function of bone marrow-derived endothelial progenitor cells in  murine liver fibrosis.

Biosci Trends. 2011 Apr;5(2):77-82

Authors: Shirakura K, Masuda H, Kwon SM, Obi S, Ito R, Shizuno T, Kurihara Y,  Mine T, Asahara T

Liver fibrosis (LF) caused by chronic liver damage has been considered as an  irreversible disease. As alternative therapy for liver transplantation, there  are high expectations for regenerative medicine of the liver.

Bone marrow (BM)-  or peripheral blood-derived stem cells, including endothelial progenitor cells  (EPCs), have recently been used to treat liver cirrhosis. We investigated the  biology of BM-derived EPC in a mouse model of LF. C57BL/6J mice were  subcutaneously injected with carbon tetrachloride (CCl4)  every 3 days for 90 days. Sacrificed 2 days after final injection, whole blood  (WB) was collected for isolation of mononuclear cells (MNCs) and biochemical  examination.

Assessments of EPC in the peripheral blood and BM were performed by  flow cytometry and EPC colonyforming assay, respectively, using purified MNCs  and BM c-KIT+, Sca-1+, and  Lin- (KSL) cells.

Liver tissues underwent histological  analysis with hematoxylin/eosin/Azan staining, and spleens were excised and  weighed. CCl4-treated mice exhibited histologically  bridging fibrosis, pseudolobular formation, and splenomegaly, indicating  successful induction of LF.

The frequency of definitive EPC-colony-forming-units  (CFU) as well as total EPC-CFU at the equivalent cell number of 500 BM-KSL cells  decreased significantly (p < 0.0001) in LF mice compared with control mice;  no significant changes in primitive EPC-CFU occurred in LF mice.

The frequency  of WB-MNCs of definitive EPC-CFU decreased significantly (p < 0.01) in LF  mice compared with control mice. Together, these findings indicated the  existence of impaired EPC function and differentiation in BM-derived EPCs in LF  mice and might be related to clinical LF.

PMID: 21572251 [PubMed - in process]

Related Articles Burden of Diarrhea in the Eastern Mediterranean Region, 1990-2013: Findings from the Global Burden of Disease Study 2013. Am J Trop Med Hyg. 2016 Dec 07;95(6):1319-1329 Authors: Khalil I, Colombara DV, Forouzanfar MH, Troeger C, Daoud F, Moradi-Lakeh M, Bcheraoui CE, Rao PC, Afshin A, Charara R, Abate KH, Razek MM, Abd-Allah F, Abu-Elyazeed R, Kiadaliri AA, Akanda AS, Akseer N, Alam K, Alasfoor D, Ali R, AlMazroa MA, Alomari MA, Al-Raddadi RM, Alsharif U, Alsowaidi S, Altirkawi KA, Alvis-Guzman N, Ammar W, Antonio CA, Asayesh H, Asghar RJ, Atique S, Awasthi A, Bacha U, Badawi A, Barac A, Bedi N, Bekele T, Bensenor IM, Betsu BD, Bhutta Z, Abdulhak AA, Butt ZA, Danawi H, Dubey M, Endries AY, Faghmous ID, Farid T, Farvid MS, Farzadfar F, Fereshtehnejad SM, Fischer F, Fitchett JR, Gibney KB, Ginawi IA, Gishu MD, Gugnani HC, Gupta R, Hailu GB, Hamadeh RR, Hamidi S, Harb HL, Hedayati MT, Hsairi M, Husseini A, Jahanmehr N, Javanbakht M, Jibat T, Jonas JB, Kasaeian A, Khader YS, Khan AR, Khan EA, Khan G, Khoja TA, Kinfu Y, Kissoon N, Koyanagi A, Lal A, Latif AA, Lunevicius R, Razek HM, Majeed A, Malekzadeh R, Mehari A, Mekonnen AB, Melaku YA, Memish ZA, Mendoza W, Misganaw A, Mohamed LA, Nachega JB, Nguyen QL, Nisar MI, Peprah EK, Platts-Mills JA, Pourmalek F, Qorbani M, Rafay A, Rahimi-Movaghar V, Rahman SU, Rai RK, Rana SM, Ranabhat CL, Rao SR, Refaat AH, Riddle M, Roshandel G, Ruhago GM, Saleh MM, Sanabria JR, Sawhney M, Sepanlou SG, Setegn T, Sliwa K, Sreeramareddy CT, Sykes BL, Tavakkoli M, Tedla BA, Terkawi AS, Ukwaja K, Uthman OA, Westerman R, Wubshet M, Yenesew MA, Yonemoto N, Younis MZ, Zaidi Z, Zaki ME, Rabeeah AA, Wang H, Naghavi M, Vos T, Lopez AD, Murray CJ, Mokdad AH Abstract Diarrheal diseases (DD) are leading causes of disease burden, death, and disability, especially in children in low-income settings. DD can also impact a child's potential livelihood through stunted physical growth, cognitive impairment, and other sequelae. As part of the Global Burden of Disease Study, we estimated DD burden, and the burden attributable to specific risk factors and particular etiologies, in the Eastern Mediterranean Region (EMR) between 1990 and 2013. For both sexes and all ages, we calculated disability-adjusted life years (DALYs), which are the sum of years of life lost and years lived with disability. We estimate that over 125,000 deaths (3.6% of total deaths) were due to DD in the EMR in 2013, with a greater burden of DD in low- and middle-income countries. Diarrhea deaths per 100,000 children under 5 years of age ranged from one (95% uncertainty interval [UI] = 0-1) in Bahrain and Oman to 471 (95% UI = 245-763) in Somalia. The pattern for diarrhea DALYs among those under 5 years of age closely followed that for diarrheal deaths. DALYs per 100,000 ranged from 739 (95% UI = 520-989) in Syria to 40,869 (95% UI = 21,540-65,823) in Somalia. Our results highlighted a highly inequitable burden of DD in EMR, mainly driven by the lack of access to proper resources such as water and sanitation. Our findings will guide preventive and treatment interventions which are based on evidence and which follow the ultimate goal of reducing the DD burden. PMID: 27928080 [PubMed - indexed for MEDLINE]
Read more...
Related Articles Common chemotherapeutic agents modulate fatty acid distribution in human hepatocellular carcinoma and colorectal cancer cells. Bioimpacts. 2017;7(1):31-39 Authors: Mehdizadeh A, Bonyadi M, Darabi M, Rahbarghazi R, Montazersaheb S, Velaei K, Shaaker M, Somi MH Abstract Introduction: Cancer cells are critically correlated with lipid molecules, particularly fatty acids, as structural blocks for membrane building, energy sources, and related signaling molecules. Therefore, cancer progression is in direct correlation with fatty acid metabolism. The aim of this study was to investigate the potential effects of common chemotherapeutic agents on the lipid metabolism of hepatocellular carcinoma (HCC) and colorectal cancer (CRC) cells, with a focus on alterations in cellular fatty acid contents. Methods: Human HepG2 and SW480 cell lines as HCC and CRC cells were respectively cultured in RPMI-1640 medium supplemented with non-toxic doses of 5-fluorouracil and doxorubicin for 72 hours. Oil Red O dye was used to estimate intracellular lipid vacuole intensity. Fatty acid analysis of isolated membrane phospholipids and cytoplasmic triglycerides (TG) was performed by gas-liquid chromatography (GLC) technique. Results: Oil red O staining represented significantly higher lipid accumulation and density in cancer cells after exposure to the chemotherapeutic agents as compared to non-treated control cells. Doxorubicin and 5-fluorouracil treatment promoted the channeling of saturated fatty acids (SFAs) from phospholipids to triglyceride pool in both HepG2 (+5.91% and +8.50%, P < 0.05, respectively) and SW480 (+37.41% and +5.73%, P < 0.05, respectively) cell lines. However, total polyunsaturated fatty acid content was inversely shifted from TG to phospholipid fraction after doxorubicin and 5-fluorouracil incubation of HepG2 (+58.89% and +29.13%, P < 0.05, respectively) and SW480 (+19.20% and +14.65%, P < 0.05, respectively) cells. Conclusion: Our data showed that common chemotherapeutic agents of HCC and CRC can induce significant changes in cellular lipid accumulation and distribution of fatty acids through producing highly saturated and unsaturated lipid droplets and membrane lipids, respectively. These metabolic side effects may be associated with gastrointestinal cancers treatment failure. PMID: 28546951 [PubMed]
Read more...

Quick Contact Form