Effect of helium-neon laser on the limbal zone cells of human eye

2015 ◽  
Vol 9 (1) ◽  
pp. 0-0
Author(s):  
Сабурова ◽  
I. Saburova ◽  
Копаева ◽  
V. Kopaeva ◽  
Копаев ◽  
...  

Currently, a helium-neon laser is widely used in the treatment of degenerative, inflammatory and vascular diseases of the eye. It was found that the interaction of this radiation with different tissues, as a result of complex photochemical processes, is manifested by anti-inflammatory, desensitizing, resolving effects. Also, there is a stimulating effect on the processes of reparation and trophism. However, these observations relate to the use of laser for external irradiation, when the light goes through the air and the sclera or through the cornea. Research of the effect of endo-laser direct exposure of the fiber in the cavity of the eye, where light acts directly on epithelial or limbal cells, wasn’t carry out due to objective reasons (difficulty of conducting such research directly to patients). There is currently no data on the effect of helium-neon laser on the limbal area of the eye-ball, enriched endogenous stem and progenitor cells. They help repair damaged tissues in the eye (anterior and posterior segment) at various injuries. Cell culture, grown in vitro, are free from the influences of body systems, attract researchers as a unique model to study the behavior of cells in normal but also in response to external or internal factors. Currently, scientists have learned how to obtain and difficult to cultivate a culture of cells, in-cluding tissues of the human eye. They are genetically homogeneous population of cells growing in constant conditions. The viability and morphology of cells and their ultra-structure and various molecular biological cha-racteristics can be studied in cell culture, and to find the optimal conditions of laser irradiation, does not damage the cells. In the present work the authors studied the effect of low-energy helium-neon laser irradiation (632 nm) on limbal stem cells. Conducted in vitro studies have shown that the use of low-energy helium-neon laser irrad-iation (632 nm) has a positive effect on the monolayer culture of limbal stem cells. Absence of changes in cell phenotype and high proliferative activity indicate a stimulating effect of the investigated radiation on stem and progenitor cells, leading to the result of the activation of recovery and reduction of pathological changes at the cellular and organ and tissue levels.

1988 ◽  
Vol 8 (2) ◽  
pp. 125-129 ◽  
Author(s):  
H. O. Hallman ◽  
J. R. Basford ◽  
John F. O'Brien ◽  
Laura A. Cummins

1990 ◽  
Vol 94 (6) ◽  
pp. 822-826 ◽  
Author(s):  
Ann F. Haas ◽  
R. Rivkah Isseroff ◽  
Ronald G. Wheeland ◽  
Pamela A. Rood ◽  
Phillip J. Graves

Author(s):  
Omika Katoch ◽  
Mrinalini Tiwari ◽  
Namita Kalra ◽  
Paban K. Agrawala

AbstractDiallyl sulphide (DAS), the pungent component of garlic, is known to have several medicinal properties and has recently been shown to have radiomitigative properties. The present study was performed to better understand its mode of action in rendering radiomitigation. Evaluation of the colonogenic ability of hematopoietic progenitor cells (HPCs) on methocult media, proliferation and differentiation of hematopoietic stem cells (HSCs), and transplantation of stem cells were performed. The supporting tissue of HSCs was also evaluated by examining the histology of bone marrow and in vitro colony-forming unit–fibroblast (CFU-F) count. Alterations in the levels of IL-5, IL-6 and COX-2 were studied as a function of radiation or DAS treatment. It was observed that an increase in proliferation and differentiation of hematopoietic stem and progenitor cells occurred by postirradiation DAS administration. It also resulted in increased circulating and bone marrow homing of transplanted stem cells. Enhancement in bone marrow cellularity, CFU-F count, and cytokine IL-5 level were also evident. All those actions of DAS that could possibly add to its radiomitigative potential and can be attributed to its HDAC inhibitory properties, as was observed by the reversal radiation induced increase in histone acetylation.


LASER THERAPY ◽  
1991 ◽  
Vol 3 (1) ◽  
pp. 25-33 ◽  
Author(s):  
J. Rigau ◽  
M.A. Trelles ◽  
R.G. Calderhead ◽  
E. Mayayo

1995 ◽  
Vol 3 (4) ◽  
pp. 512-517 ◽  
Author(s):  
Caroline Broadley ◽  
Kenneth N. Broadley ◽  
Gerald Disimone ◽  
Lou Reinisch ◽  
Jeffrey M. Davidson

Blood ◽  
2002 ◽  
Vol 99 (1) ◽  
pp. 15-23 ◽  
Author(s):  
James C. Mulloy ◽  
Jörg Cammenga ◽  
Karen L. MacKenzie ◽  
Francisco J. Berguido ◽  
Malcolm A. S. Moore ◽  
...  

The acute myelogenous leukemia–1 (AML1)–ETO fusion protein is generated by the t(8;21), which is found in 40% of AMLs of the French-American-British M2 subtype. AML1-ETO interferes with the function of the AML1 (RUNX1, CBFA2) transcription factor in a dominant-negative fashion and represses transcription by binding its consensus DNA–binding site and via protein-protein interactions with other transcription factors. AML1 activity is critical for the development of definitive hematopoiesis, and haploinsufficiency of AML1 has been linked to a propensity to develop AML. Murine experiments suggest that AML1-ETO expression may not be sufficient for leukemogenesis; however, like the BCR-ABL isoforms, the cellular background in which these fusion proteins are expressed may be critical to the phenotype observed. Retroviral gene transfer was used to examine the effect of AML1-ETO on the in vitro behavior of human hematopoietic stem and progenitor cells. Following transduction of CD34+ cells, stem and progenitor cells were quantified in clonogenic assays, cytokine-driven expansion cultures, and long-term stromal cocultures. Expression of AML1-ETO inhibited colony formation by committed progenitors, but enhanced the growth of stem cells (cobblestone area-forming cells), resulting in a profound survival advantage of transduced over nontransduced cells. AML1-ETO–expressing cells retained progenitor activity and continued to express CD34 throughout the 5-week long-term culture. Thus, AML1-ETO enhances the self-renewal of pluripotent stem cells, the physiological target of many acute myeloid leukemias.


Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 2207-2207
Author(s):  
Ashu Kumari ◽  
Cornelia Brendel ◽  
Thorsten Volkmann ◽  
Sonja Tajstra ◽  
Andreas Neubauer ◽  
...  

Abstract Abstract 2207 Poster Board II-184 Introduction: Treatment with the Abl-kinase specific inhibitor imatinib (IM) is very effective in chronic myeloid leukemia (CML). However, IM presumably fails to eradicate CML stem cells (HSC) leading to disease persistence and relapse after IM-discontinuation. Although causes of CML persistence under imatinib remain ill defined, quiescence and BCR/ABL-overexpression of CML stem and progenitor cells have been suggested as underlying mechanisms. We here set out to identify means to directly study persistence mechanisms in residual BCR/ABL-positive progenitor and stem cell clones from chronic phase CML patients in major molecular remission (mmR) under imatinib. Methods: Bone marrow specimens of twenty-one CML patients in at least major molecular remission (mmR) according to the international scale, first diagnosis (FD) patients (n=5) and healthy donors (n=4) were sorted into HSC, common myeloid progenitors (CMP), granulocyte/macrophage progenitors (GMP) and megakaryocate-erythrocyte progenitors (MEP) and BCR-ABL mRNA expression was directly assessed by quantitative real time (qPCR) and/or nested PCR (mRNA of 4.000 sorted cells). Alternatively, HSC, CMP, GMP and MEP were seeded into soft agar and mRNA was extracted from individual colony forming units (CFU) to assess BCR/ABL-mRNA expression by qPCR. Moreover, CFU of sub-fractions of first diagnosis CML patients were treated in vitro with IM at 3mM and BCR/ABL-expression of surviving CFU was compared with the BCR/ABL expression levels of mock-treated CML-CFU. In total, 595 soft agar colonies were analyzed. Results: By nested PCR, BCR/ABL-mRNA was readily detectable in the HSC compartments of 7 of 10 (7/10) CML patients in mmR. BCR/ABL was also detected in the CMP-, GMP-, and MEP-compartments in 6, 10 and 8 of the 10 patients, respectively. Real time qRT-PCR suggested only a trend toward stronger BCR/ABL positivity of the HSC compartment when compared to the other progenitor compartments (table 1). A detailed analysis of the BCR/ABL-expression of individual CFU from HSC-, CMP-, GMP-, and MEP-compartments of mmR patients revealed that persisting CML-CFU expressed significantly less BCR/ABL than first diagnosis CML-CFU obtained before imatinib therapy (table 1). This finding could be recapitulated in vitro: primary CML-CD34+ cells of first diagnosis CML patients (n=4) were seeded into soft agar in the presence or absence of 3 uM imatinib. After 14 days BCR/ABL expression only of BCR/ABL-positive CFU was compared. BCR/ABL-positive CML-CFU (n=30) that had survived imatinib exposure expressed significantly less BCR/ABL than mock-treated CML-CFU (n=175) (p<0.001). Work is in progress providing in vitro evidence that selection/induction of low BCR/ABL expression in immature progenitor and stem cells is a new mechanism of imatinib persistence in mmR patients via reducing oncogenic addiction from BCR/ABL. Conclusions: We showed that BCR/ABL-persistence is not confined to the quiescent CML-stem cell compartment, but seems to affect also the highly proliferative progenitor compartments. More intriguingly, persisting CML-HSC and -precursor cells express remarkably low levels of BCR/ABL when compared to first diagnosis HSC and progenitors, implying that low BCR/ABL expression reduces imatinib sensitivity in vivo. The simple model of selection / induction of low BCR/ABL expression as mechanism of imatinib persistence in CML would explain the low propensity of disease progression after achieving mmR, and the low genetic instability of CML clones from mmR patients. Disclosures: No relevant conflicts of interest to declare.


Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 2047-2047
Author(s):  
Wendy Pang ◽  
Elizabeth Price ◽  
Irving L. Weissman ◽  
Stanley L. Schrier

Abstract Abstract 2047 Anemia is both a highly prevalent and clinically important condition that causes significant morbidity and mortality in the elderly population. While anemia in the elderly can be attributed to a number of causes, approximately 30% of elderly subjects with anemia have no overt etiology and fall under the category of unexplained anemia of the elderly (UA). There is increasing evidence to suggest that changes in the frequency and/or function of hematopoietic stem and progenitor cells may contribute to the onset and pathophysiology of age-associated hematological conditions, such as UA. Hematopoietic stem cells (HSC) reside at the top of the hematopoietic hierarchy and can differentiate, via increasingly committed downstream progenitors, into all the mature cells of the hematopoietic system. Human myelo-erythroid development proceeds through a set of oligopotent progenitors: HSC give rise to multipotent progenitors (MPP), which give rise to common myeloid progenitors (CMP), which in turn give rise to granulocyte-macrophage progenitors (GMP) and megakaryocyte-erythrocyte progenitors (MEP). We use flow cytometry and in vitro culture of sorted human HSC (Lin-CD34+CD38-CD90+CD45RA-), MPP (Lin-CD34+CD38-CD90-CD45RA-), CMP (Lin-CD34+CD38+CD123+CD45RA-), GMP (Lin-CD34+CD38+CD123+CD45RA+), and MEP (Lin-CD34+CD38+CD123-CD45RA-) from hematologically normal young (23 samples; age 20–35) and elderly (11 samples; age 65+) and UA (5 samples; age 65+) bone marrow samples in order to characterize the changes in the distribution and function of hematopoietic stem and progenitor populations during the aging process and, in particular, in the development of UA. We found that UA patients contain higher frequencies of HSC compared to both elderly normal (1.5-fold; p<0.03) and young normal samples (2.8-fold; p<10-5). We also found increased frequencies of MPP from UA patients compared to MPP from elderly normal (2.6-fold; p<0.002) and young normal samples (5.8-fold; p<0.04). While we observed similar frequencies of CMP among the three groups, we found a notable trend suggesting decreased frequencies of GMP and corresponding increased frequencies of MEP in UA patients. Functionally, HSC from the three groups exhibit statistically insignificant differences in the efficiency of colony formation under the myeloid differentiation-promoting methylcellulose-based in vitro culture conditions; however, on average, HSC from elderly bone marrow samples, regardless of the presence or absence of anemia, tend to form fewer colonies in methylcellulose. Interestingly, HSC from UA patients produce more granulocyte-monocyte (CFU-GM) colonies and fewer erythroid (CFU-E and BFU-E) colonies, compared to HSC from normal samples (p<0.001). Similarly, CMP from UA patients, compared to normal CMP, yield skewed distributions of myeloid-erythroid colonies when plated in methylcellulose, significantly favoring production of CFU-GM colonies over CFU-E and BFU-E colonies (p<0.003). Additionally, MEP from UA patients form both CFU-E and BFU-E colonies in methylcellulose albeit at a significantly lower efficiency than MEP from normal bone marrow samples (p<0.01). This is the first study to examine the changes in hematopoietic stem and progenitor populations in UA patients. The changes in the distribution of hematopoietic stem and progenitor cells in UA patients indicate that the HSC and MPP populations, and possibly also the MEP population, expand in the context of anemia, potentially in response to homeostatic feedback mechanisms. Nevertheless, these expanded populations are functionally impaired in their ability to differentiate towards the erythroid lineage. Our data suggest that there are intrinsic defects in the HSC population of UA patients that lead to poor erythroid differentiation, which can be readily observed even in the earliest committed myelo-erythroid progenitors. We have generated gene expression profiling data from these purified hematopoietic stem and progenitor populations from UA patients to try to identify biological pathways and markers relevant to disease pathogenesis and potential therapeutic targets. Disclosures: Weissman: Amgen, Systemix, Stem cells Inc, Cellerant: Consultancy, Employment, Equity Ownership, Membership on an entity's Board of Directors or advisory committees. Schrier:Celgene: Research Funding.


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