scholarly journals How Should an Increase in Alkaline Phosphatase Activity Be Interpreted?

2007 ◽  
Vol 2007 ◽  
pp. 1-10 ◽  
Author(s):  
Denise Hawkins ◽  
Heidi Abrahamse
Keyword(s):  
Cell Proliferation ◽  
Alkaline Phosphatase ◽  
Enzyme Activity ◽  
Optical Density ◽  
Membrane Integrity ◽  
Cellular Responses ◽  
Neutral Red ◽  
Cellular Damage ◽  
Low Level Laser Therapy

Low-level laser therapy, commonly known as LLLT, is the application of low power, monochromatic, and coherent light to injuries and lesions to stimulate healing and give pain relief. There are conflicting reports in the literature regarding the role of ALP. Objective: this study aimed to compare the cellular responses of wounded human skin fibroblasts exposed to doses of 0.5 J/cm2, 2.5 J/cm2, 5 J/cm2, or 16 J/cm2 using LLLT with a Helium-Neon laser (632.8 nm, 18.8 mW power output, 2.07 mW/cm2 power density, and 3.4 cm diameter spot size or area 9.1 cm2) to elucidate the role of alkaline phosphatase (ALP) in cell proliferation. Methods: cellular responses to laser irradiation were evaluated using ALP enzyme activity, LDH membrane integrity, neutral red for cell proliferation, optical density at 540 nm, and basic fibroblast growth factor (bFGF) expression. Results: results suggest that an increase in ALP is negatively correlated with cell growth depending on the concentration of growth factors in the medium. Results also indicate that an increase in ALP may be related to cellular damage. Conclusion: since the exact role of ALP is unknown, the ALP enzyme activity assay should be considered in conjunction with other cell proliferation assays such as neutral red, optical density, or more specifically bFGF expression.

The reopening process of the esophagus in the normal chick and the crookedneck dwarf mutant

Development ◽  
1966 ◽  
Vol 15 (1) ◽  
pp. 67-76
Author(s):  
Allan L. Allenspach
Keyword(s):  
Cell Proliferation ◽  
Alkaline Phosphatase ◽  
Ribonucleic Acid ◽  
Dwarf Mutant ◽  
Histological Changes ◽  
Acid And Alkaline Phosphatase

In an earlier publication (Allenspach & Hamilton, 1962) an account was given of chick esophageal development and histogenesis up to 10 days of incubation. The esophagus becomes completely occluded at 5 days (stage 26, Hamburger & Hamilton, 1951) and reopens rapidly at 7½–8 days (stages 33–34). Detailed observations were made of the histological changes in the organs as correlated with the localization of ribonucleic acid and alkaline phosphatase. The occlusion of the developing esophagus was apparently due to collapse and adhesion of roof and floor epithelia to form a solid epithelial bar and not to cell proliferation, as stated in Lillie's Development of the Chick (Hamilton, 1952, pp. 384–5). This process was the object of further investigation in which the role of proliferation in occlusion was determined by the use of colchicine. Results indicated that cell proliferation is not involved in the closing process (Allenspach, 1964).

Precocious and reversible expression of sucrase-isomaltase unrelated to intestinal cell turnover

1994 ◽  
Vol 266 (4) ◽  
pp. G568-G575 ◽  
Author(s):  
E. Nsi-Emvo ◽  
C. Foltzer-Jourdainne ◽  
F. Raul ◽  
F. Gosse ◽  
I. Duluc ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Alkaline Phosphatase ◽  
Enzyme Activity ◽  
Epithelial Cell ◽  
Serum Level ◽  
Intestinal Cell ◽  
Epithelial Cell Proliferation ◽  
Cell Turnover ◽  
Sucrase Activity ◽  
Intestinal Sucrase

The effect of starvation and refeeding on the developmental pattern of intestinal sucrase-isomaltase (SI) was analyzed in preweaned rats. Starvation at postnatal day 12 caused a precocious expression of SI activity and mRNA. Alkaline phosphatase activity was slightly reduced, and no significant change was observed for aminopeptidase and lactase activities. Immunostaining showed that SI molecules appear in cells at the base of the villus. Sucrase expression was further increased by prolonged food deprivation, whereas enzyme activity as well as the amount of SI mRNA dropped to reach the low level found in control sucklings when 48 h-starved pups were refed by returning them to their dams. During the refeeding period, the enterocytes that were committed to produce SI by starvation continued to express the enzyme while migrating up the villi. However, the new epithelial cells arising from the crypts no longer synthesized the disaccharidase. The starvation-evoked appearance of SI was preceded by a transient burst of expression of the protooncogene c-fos, an event that may be correlated to the ontogenic rise of c-fos mRNA observed before weaning. However, in contrast to the normal weaning condition, SI induction by starvation occurred without obvious increase of epithelial cell proliferation and turnover. During the starvation and refeeding period, patterns of sucrase activity and SI mRNA paralleled the serum level of glucocorticoids.(ABSTRACT TRUNCATED AT 250 WORDS)

TRIM44 promotes cell proliferation and migration by inhibiting FRK in renal cell carcinoma

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Lymphatic Invasion ◽  
Cancer Specific Survival ◽  
Candidate Target ◽  
Candidate Target Gene ◽  
And Migration

TRIM44 has oncogenic roles in various cancers. However, TRIM44 expression andits function in renal cell carcinoma (RCC) are still unknown. Here in this study, weinvestigated the clinical significance of TRIM44 and its biological function in RCC.TRIM44 overexpression was significantly associated with clinical M stage, histologictype (clear cell) and presence of lymphatic invasion (P = .047, P = .005, and P = .028,respectively). Moreover, TRIM44 overexpression was significantly associated withpoor prognosis in terms of cancer-specific survival (P = .019). Gain-of-function andloss-of-function studies using TRIM44 and siTRIM44 transfection showed thatTRIM44 promotes cell proliferation and cell migration in two RCC cell lines, Caki1and 769P. To further investigate the role of TRIM44 in RCC, we performed integratedmicroarray analysis in Caki1 and 769P cells and explored the data in the Oncominedatabase. Interestingly, FRK was identified as a promising candidate target gene ofTRIM44, which was downregulated in RCC compared with normal renal tissues. Wefound that cell proliferation was inhibited by TRIM44 knockdown and then recoveredby siFRK treatment. Taken together, the present study revealed the associationbetween high expression of TRIM44 and poor prognosis in

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