Haematology of cultured Murray cod

Murray cod are Australia's largest freshwater fish: endangered in the wild, but supporting a boutique industry. This project studied the blood cells of Murray cod and those affected by the disfiguring chronic erosive dermatopathy. This has provided insight into the factors affecting Murray cod health.

Blood cells of Murray cod maccullochella peelii peelii (Mitchell)

Analysis of the peripheral blood cells of Murray cod Maccullochella peelii peelii identified seven distinct subpopulations including a novel basophilic cell. Haematological reference ranges were established to facilitate future diagnostic blood sampling of this fish.

G-CSF: function and modes of action (Review)

Since the observations in the 1960s that granulocyte-colony stimulating factor (G-CSF) stimulated the proliferation of granulocytic cells in semisolid cultures of bone marrow cells, G-CSF has established itself as a useful clinical agent for increasing levels of neutrophilic granulocytes. However, these early findings did not firmly establish whether G-CSF is a genuine regulator of granulocyte formation under normal physiological conditions or rather acts as an emergency regulator, playing an important role only under stress conditions. The advent of <gene-knockout technology> has allowed us to evaluate these questions in a physiological setting through analysis of mice with a targeted mutation of G-CSF or its receptor, while the development of relevant cell models has enabled us to dissect the molecular basis of G-CSF action. This review discusses our current state of knowledge regarding the role of G-CSF in granulopoiesis.

Somatostatin modulates G-CSF-induced but not interleukin-3-induced proliferative responses in myeloid 32D cells via activation of somatostatin receptor subtype 2

Somatostatin, originally identified as a peptide involved in neurotransmission, functions as an inhibitor of multiple cellular responses, including hormonal secretion and proliferation. Somatostatin acts through activation of G-protein-coupled receptors of which five subtypes have been identified. We have recently established that human CD34/c-kit expressing hematopoietic progenitors and acute myeloid leukemia (AML) cells exclusively express SSTR2. A major mechanism implicated in the antiproliferative action of somatostatin involves activation of the SH2 domain-containing protein tyrosine phosphatase SHP-1. While 0.1-1 x 10(-9) M of somatostatin, or its synthetic stable analog octreotide, can inhibit G-CSF-induced proliferation of AML cells, little or no effects are seen on GM-CSF- or IL-3-induced responses.
MATERIALS AND METHODS: To study the mechanisms underlying the antiproliferative responses of myeloblasts to somatostatin, clones of the IL-3-dependent murine cell line 32D that stably express SSTR2 and G-CSF receptors were generated. RESULTS: Similar to AML cells, octreotide inhibited G-CSF-induced but not IL-3-induced proliferative responses of 32D[G-CSF-R/SSTR2] cells. Somatostatin induced SHP-1 activity and inhibited G-CSF-induced, but not IL-3-induced, activation of the signal transducer and activator of transcription proteins STAT3 and STAT5.
CONCLUSION: Based on these data and previous results, we propose a model in which recruitment and activation of the tyrosine phosphatase SHP-1 by SSTR2 is involved in the selective negative action of somatostatin on G-CSF-R signaling.