Differential expression of peroxiredoxin subtypes in human brain cell types

Abstract

The peroxiredoxin (Prx) protein is expressed widely in animal tissues and serves an antioxidant function associated with removal of cellular peroxides. We have cloned two Prx genes and observed differential expression of Prx-I and Prx-II (formerly NKEF-A and NKEF-B) in purified rat brain cell cultures (Sarafian et al. [1998] Mol. Chem. Neuropathol. 34:39-51). We have examined regional and cell-type-specific expression of Prx-I and Prx-II in paraffin sections of human brain using immunohistochemical methods. These studies revealed a clear segregation of expression of these two gene products in different brain cell types. In the cerebral cortex, cerebellum, basal ganglia, substantia nigra, and spinal cord, Prx-I was expressed primarily in astrocytes, while Prx-II was expressed exclusively in neurons. Prx-I was also prominently expressed in ependymal cells and subependymal matrix of substantia nigra and basal ganglia. Prx-II was not expressed at uniform density in all neurons. In general, small neurons such as cerebellar granule neurons displayed little or no staining, while large neurons, such as hippocampal pyramidal and Purkinje neurons were heavily stained. The absence of expression of Prx-I in neurons and the selective expression of Prx-II in large neurons suggest that these antioxidant enzymes serve distinct functional roles that may reflect the different functions and biochemical activities of these cell types. Restricted expression of these genes may also contribute to the selective vulnerability of these cells to a wide variety of neuropathologic conditions.

Induction of radioprotective peroxiredoxin‐I by ionizing irradiation

“…The discrepancy between the two studies may be due to the types of cell lines used. As we have reported Sarafian et al, 1999), Prx-I and -II expression patterns vary greatly between tissues. The response to stimulation would similarly be expected to vary between different cell types.…”

“…After protein quantification (Micro-BCA Protein Assay; Pierce, Rockford, IL), 20 g of protein per lane were loaded on 4 -12% sodium dodecyl sulfate (SDS)-polyacrylamide gels, electrophoresed, and transferred to polyvinylidene difluoride (PVDF) membranes (Bio-Rad, Hercules, CA). The membranes were blocked at 4°C overnight with TBS buffer [Tris-buffered saline, pH 7.5, containing 2% fetal bovine serum (FBS) and 0.1% Tween 20], and then probed with anti-human Prx-I or -II mouse monocloncal antibody (mAbs) as previously described Sarafian et al, 1999). Resulting protein bands were quantified using the NIH Image software.…”

Cytosolic proteomic alterations in the nucleus accumbens of cocaine overdose victims

“…Like PRDX1, PRDX2 is a highly abundant cytosolic protein and is a primary regulator of H 2 O 2 generated by cell surface receptors. 93 PRDX2 is expressed in neurons but not in glial cells 94 and appears to be located primarily in cells vulnerable to oxidative stress and ischemic injury, such as the hippocampus and cerebellum. 94 PRDX2 provides an important function by protecting protein and lipids against oxidative injury 95,96 and regulates apoptosis 97 by eliminating peroxides generated during metabolism.…”

“…Figure 5a is representative of protein identification in this study. The GFAP identification was validated by sequencing two peptides, ALAAELNQLR [94][95][96][97][98][99][100][101][102][103] and LADVYQAELR, [110][111][112][113][114][115][116][117][118][119] having precursor ion m/z of 1098.6 and 1177.6, respectively (Figure 5b and c). Some of the protein spots that yielded significant DeCyder ratios were not identified with MALDI-ToF-MS, which can be attributed to insufficient amounts of protein.…”

Oxidative and nitrosative stress induces peroxiredoxins in pancreatic beta cells

“…It also regulates signal transduction pathways that directly relate to apoptotic cell death [23,27,28,29,46]. Prx II is thought to protect neuronal cells against destruction by hypoxia and ischaemia [11,47] and tumour cells against X-ray treatment and chemotherapy [48].…”