Biomedical subjects

M Blass

Publications and source records attributed to M Blass.

3 recordsLinked to original sources

PubMed2001

Protein kinase Calpha and protein kinase Cdelta play opposite roles in the proliferation and apoptosis of glioma cells.

Protein kinase C (PKC) has been implicated in the proliferation and apoptosis of glial tumors, but the role of specific PKC isoforms remains unresolved. Comparing brain tumors differing in degree of malignancy, we found that malignant gliomas expressed higher levels of PKCalpha and lower levels of PKCdelta as compared with low-grade astrocytomas. Consistent with a mechanistic role for these differences, overexpression of PKCalpha in the human U87 glioma cell line resulted in enhanced cell proliferation and decreased glial fibrillary acidic protein (GFAP) expression as compared with controls. Reciprocally, overexpression of PKCdelta inhibited cell proliferation and enhanced GFAP expression. Using PKC chimeras, we found that the regulatory domains of PKCalpha and PKCdelta mediated their effects on cell proliferation and GFAP expression. PKCalpha and delta have been implicated as potential signaling molecules in apoptosis. Therefore, we examined the role of these isoforms in the resistance of glioma cells to apoptotic stimuli. In U87 cells, manipulation of PKCalpha levels had little effect on apoptosis in response to etoposide. In contrast, overexpression of PKCdelta rendered the U87 cells more sensitive to the apoptotic effect of etoposide, and PKCdelta was cleaved in these cells by a caspase-dependent process. Furthermore, the glioma cell line U373, which expresses endogenous PKCdelta, underwent apoptosis in response to etoposide, and the apoptotic response was blocked by the PKCdelta inhibitor rottlerin. Our results suggest that PKCalpha and PKCdelta play opposite roles in the proliferation and apoptosis of glioma cells.

Antineoplastic Agents, Phytogenic↗

PubMed2000

Apoptosis induction of human myeloid leukemic cells by ultrasound exposure.

Therapeutic ultrasound (ULS) and the resulting cavitation process has been shown to induce irreversible cell damage. In this study, we wanted to further investigate the mechanism of ULS-induced cell death and to determine whether apoptosis is involved. High intensity focused pulsed ULS sonication at a frequency of 750 KHz was delivered to HL-60, K562, U937, and M1/2 leukemia cell line cultures. ULS exposure used with induction of transient cavitation in the focal area was delivered with an intensity level of 103.7 W/cm2 and 54.6 W/cm2 spatial-peak temporal-average intensity. As a control, ULS of lower intensity was delivered at 22.4 W/cm2 spatial-peak temporal-average intensity, presumably without generation of cavitation. Our results indicated that DNA damage induced by ULS cavitation did not involve generation of free radicals in the culture media. Morphological alterations observed in cells after exposure to ULS included: cell shrinkage, membrane blebbing, chromatin condensation, nuclear fragmentation, and apoptotic body formation. Apoptotic cells were evaluated by fluorescence microscopy and detected using the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay, which identifies DNA breaks, and by the leakage of phosphatidylserine from the inner to the outer side of the membrane layer of treated cells. Some bioeffects induced on sonicated HL-60 cells, such as inhibition of cell proliferation, DNA repair, and cell-dependent apoptosis, were found to be similar to those produced by gamma-irradiation. Thus, much of the cell damage induced by therapeutic ULS in leukemia cells surviving ULS exposure appears to occur through an apoptotic mechanism.

Apoptosis↗

PubMed1988

Leveraging case-mix data at Melrose-Wakefield.

Melrose-Wakefield Hospital in Melrose, Mass., is tripling space in its operating rooms, expanding ancillary services and staging areas for ambulatory patients and totally renovating its maternity section. These are healthy signs at a time when many hospitals are experiencing financial problems.

Data Collection↗