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34. Genetic analysis of type material of the Amur lemming resolves nomenclature issues and creates challenges for the taxonomy of true lemmings (Lemmus, Rodentia: Cricetidae) in the eastern Palearctic.

Author

ABRAMSON, N. I. and PETROVA, T. V.

Subjects
*ZOOLOGICAL nomenclature, *TAXONOMY, *PHYLOGENY, *MUSEUMS
Abstract

The proper use of species names depends entirely on verifying whether newly analysed specimens are conspecific with the type material. True lemmings (Lemmus) are the most common rodents of the Arctic tundra in the Old and New World and play an important role in the Arctic ecosystem; however, their taxonomy is far from resolved. The Amur lemming (L. amurensis) is the least studied and most enigmatic species of the genus. Its taxonomic position, distribution and nomenclature are uncertain due to a lack of cytogenetic, molecular phylogenetic and hybridization studies. Assignment of all true lemmings from the vast territory of western Beringia to this species has never properly been confirmed. Moreover, the type locality for this species was flooded by a newly created reservoir in 1974, making additional topotypes unavailable. In this context, genetic analysis of museum specimens, especially type material, has great potential. Here we report partial cytochrome b sequences extracted from all specimens identified as L. amurensis stored in the two largest mammal collections in Russian museums, including the holotype of L. amurensis and the type material of all forms currently considered as synonyms of L. amurensis. Phylogenetic analyses suggest that the range of the Amur lemming is dramatically smaller than previously assumed and is limited to the territories of Transbaikalia, South Yakutia and Amur in the eastern Palaearctic. Lemmus taxa from other territories, including L. amurensis ognevi and L. amurensis flavescens, refer to other lemming species. Our results impinge on nomenclature issues, taxonomy, divergence times and the evolutionary history of lemmings in the eastern part of the Palearctic and on the species concept as applied to the genus Lemmus. [ABSTRACT FROM AUTHOR]

Published
2018
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36. Molecular mechanisms of lymphatic vascular development.

Author

Mäkinen, Taija, Norrmén, C, Petrova, T V, Mäkinen, Taija, Norrmén, C, and Petrova, T V

Abstract

Lymphatic vasculature has recently emerged as a prominent area in biomedical research because of its essential role in the maintenance of normal fluid homeostasis and the involvement in pathogenesis of several human diseases, such as solid tumor metastasis, inflammation and lymphedema. Identification of lymphatic endothelial specific markers and regulators, such as VEGFR-3, VEGF-C/D, PROX1, podoplanin, LYVE-1, ephrinB2 and FOXC2, and the development of mouse models have laid a foundation for our understanding of the major steps controlling growth and remodeling of lymphatic vessels. In this review we summarize recent advances in the field and discuss how this knowledge as well as use of model organisms, such as zebrafish and Xenopus, should allow further in depth analysis of the lymphatic vascular system.

Published
2007
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40. Signalling via vascular endothelial growth factor receptor-3 is sufficient for lymphangiogenesis in transgenic mice.

Author

Veikkola, T, Jussila, L, Mäkinen, Taija, Karpanen, T, Jeltsch, M, Petrova, T V, Kubo, H, Thurston, G, McDonald, D M, Achen, M G, Stacker, S A, Alitalo, K, Veikkola, T, Jussila, L, Mäkinen, Taija, Karpanen, T, Jeltsch, M, Petrova, T V, Kubo, H, Thurston, G, McDonald, D M, Achen, M G, Stacker, S A, and Alitalo, K

Abstract

Vascular endothelial growth factor receptor-3 (VEGFR-3) has an essential role in the development of embryonic blood vessels; however, after midgestation its expression becomes restricted mainly to the developing lymphatic vessels. The VEGFR-3 ligand VEGF-C stimulates lymphangiogenesis in transgenic mice and in chick chorioallantoic membrane. As VEGF-C also binds VEGFR-2, which is expressed in lymphatic endothelia, it is not clear which receptors are responsible for the lymphangiogenic effects of VEGF-C. VEGF-D, which binds to the same receptors, has been reported to induce angiogenesis, but its lymphangiogenic potential is not known. In order to define the lymphangiogenic signalling pathway we have created transgenic mice overexpressing a VEGFR-3-specific mutant of VEGF-C (VEGF-C156S) or VEGF-D in epidermal keratinocytes under the keratin 14 promoter. Both transgenes induced the growth of lymphatic vessels in the skin, whereas the blood vessel architecture was not affected. Evidence was also obtained that these growth factors act in a paracrine manner in vivo. These results demonstrate that stimulation of the VEGFR-3 signal transduction pathway is sufficient to induce specifically lymphangiogenesis in vivo.

Published
2001
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41. Signaling via vascular endothelial growth factor receptors.

Author

Petrova, T V, Mäkinen, Taija, Alitalo, K, Petrova, T V, Mäkinen, Taija, and Alitalo, K

Abstract

Angiogenesis, or development of blood vessels from preexisting vasculature, has important functions under both normal and pathophysiological conditions. Vascular endothelial growth factor receptors 1-3, also known as flt-1, KDR, and flt-4, are endothelial cell-specific receptor tyrosine kinases which serve as key mediators of the angiogenic responses. The review focuses on the signaling pathways that are initiated from these receptors and the recently identified VEGF coreceptor neuroplilin-1.

Published
1999
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50. Selective modulation of BV-2 microglial activation by prostaglandin E(2). Differential effects on endotoxin-stimulated cytokine induction.

Author

Petrova, T V, Akama, K T, and Van Eldik, L J

Abstract

The influence of prostaglandins on glial functions and, more specifically, on glial activation is not well understood. We report here that prostaglandin E(2) (PGE(2)), one of the major prostaglandins produced in the brain, acts as a potent and selective inhibitor of tumor necrosis factor alpha (TNF-alpha) production in lipopolysaccharide-stimulated primary microglia and the microglial cell line BV-2. The IC(50) for this effect is 1 nM, and 100 nM PGE(2) suppresses TNF-alpha production by >95%. More detailed studies of BV-2 cells show that PGE(2) also prevents the secretion of interleukin (IL)-6 but does not significantly modify lipopolysaccharide-stimulated expression of cyclooxygenase-2, pro-IL-1beta, or inducible nitric oxide synthase. PGE(2) appears to act primarily at the level of translation or protein stability, because TNF-alpha and IL-6 mRNA levels were only modestly decreased at high PGE(2) concentrations; concomitantly with this inhibition, PGE(2) up-regulated the levels of IL-1beta mRNA. The effects of PGE(2) could be largely mimicked by 8-bromo-cAMP, suggesting that, as in other cell types, PGE(2) action is mediated at least in part by a rise in intracellular cyclic AMP. However, the protein kinase A inhibitor H89 only partially reversed the inhibition of TNF-alpha production by PGE(2), implying that the PGE(2) effect in BV-2 cells is mediated through both protein kinase A-dependent and -independent pathways.

Published
1999

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