PLIF, a Novel Human Ferritin Subunit from Placenta with Immunosuppressive Activity

Moroz, Chaya; Traub, Leonid; Maymon, Ron; Zahalka, Muayad A.

doi:10.1074/jbc.m200956200

Cited by 20 publications

(34 citation statements)

References 19 publications

(17 reference statements)

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“…Furthermore, PLIF mRNA expression was also found in human liver (Moroz et al, 2002). Taken together this suggests, that PLIF, produced by rat hepatocytes may represent the source for the apoptosis inducing activity of CM 0-3 .…”

Section: Discussionmentioning

confidence: 74%

Induction of apoptosis by a hepatocyte conditioned medium

Bresgen¹,

Rolinek²,

Hochleitner³

et al. 2003

Journal Cellular Physiology

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Incubation of primary cultures of parenchymal hepatocytes in a conditioned medium (CM), collected over the first 3 h of serum-free rat hepatocyte culture (CM(0-3)), induces a time dependent increase of the frequency of apoptotic cells which is accompanied by prominent changes of cell morphology. Short-term treatment with CM(0-3) for the first 3 h of culture is sufficient to significantly (P < 0.05) increase the frequency of apoptotic cells, however, the effect is more pronounced upon long-term treatment. Although apoptosis induction by CM(0-3) is independent of the timepoint when cultivation in CM(0-3) starts, our results suggest that the sensitivity for apoptosis induction by CM(0-3) is increased during the phase of attachment. Purification of CM(0-3) resulted in a fraction which significantly (P < 0.05) induced apoptosis at concentrations >/=10 ng/ml. Exposure of cultures to concentrations >/=1 microg/ml of purified CM(0-3) gave rise to a prominent cytotoxic effect as indicated by the massive occurrence of necrotic cells. Biochemical analysis showed that the purified fraction of CM(0-3) contains acidic ferritins with molecular weight of 23 and 43 kDa. Strikingly, both share homologies with placental isoferritins (PLF), for which growth inhibitory and immunosuppressive effects have been demonstrated by several investigations. Therefore, our results provide evidence that rat hepatocytes produce PLF or PLF-related acidic isoferritins which are able to induce apoptosis.

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Section: Discussionmentioning

confidence: 74%

Induction of apoptosis by a hepatocyte conditioned medium

Bresgen¹,

Rolinek²,

Hochleitner³

et al. 2003

Journal Cellular Physiology

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“…Hence, the host iron status and the progression of viral infection seem to be strictly connected. In this scenario, it is noteworthy to consider that ferritin induction during infection could play a pivotal role in immunosuppressive mechanisms, acting as a down-regulator of cellular immunity [Moroz et al, 1989[Moroz et al, , 2002. Should be this the case, the enhanced ferritin content found in the MDBK cells upon BHV-1 infection would correlate with the suppression of the antiviral host cell response.…”

Section: Discussionmentioning

confidence: 97%

Expression of iron‐related proteins during infection by bovine herpes virus type‐1

Maffettone

Martino

Irace

et al. 2007

J of Cellular Biochemistry

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Bovine herpesvirus 1 (BHV-1), a dsDNA animal virus, is an economically important pathogen of cattle and the aetiological agent of many types of disease. The efficient replication of a DNA virus is strictly dependent on iron since this metal plays a crucial role in the catalytic center of viral ribonucleotide reductase. Consequently, iron metabolism is an important area for virus/host interaction and a large body of evidence suggests that viral infection is potentially influenced by the iron status of the host. The aim of the present study was to address the effects of BHV-1 on iron metabolism in Madin-Darby bovine kidney (MDBK) cells at different times of post-infection. For this purpose, cell viability, iron regulatory proteins (IRPs) activity and levels, transferrin receptor 1 (TfR-1), ferritin expression and LIP were evaluated. Our data demonstrate that a productive BHV-1 infection in MDBK cells determines an overall decrease of IRPs RNA-binding activity without affecting their expression. As consequence of this modulation, an increased ferritin mRNA translation and a decreased TfR-1 mRNA translation were also observed. Moreover, the LIP level was decreased following viral infection. These results are consistent with the hypothesis that by reducing the iron up-take and by enhancing the sequestration of free iron, animal cells will limit the iron availability for virus proliferation. Therefore, the results presented herein support the view that iron metabolism could be critical for the interaction between DNA viruses, such as BHV-1, and mammalian cells. Delineation of the interplay among pathogen and host may provide new antimicrobial agents.

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“…Placental immunomodulatory ferritin (PLIF), a protein identical to the ferritin heavy chain for the first 118 amino acids but derived from a different gene, is expressed by placental trophoblasts (Moroz et al, 2002). PLIF is not known to be involved in iron storage but has roles in immune regulation.…”

Section: Placental Architecture and Proteins Of Iron Metabolismmentioning

confidence: 99%