Smart Textiles for Visible and IR Camouflage Application: State-of-the-Art and Microfabrication Path Forward.

Protective textiles used for military applications must fulfill a variety of functional requirements, including durability, resistance to environmental conditions and ballistic threats, all while being comfortable and lightweight. In addition, these textiles must provide camouflage and concealment under various environmental conditions and, thus, a range of wavelengths on the electromagnetic spectrum. Similar requirements may exist for other applications, for instance hunting.

β-Cells with relative low HIMP1 overexpression levels in a transgenic mouse line enhance basal insulin production and hypoxia/hypoglycemia tolerance.

Rodent pancreatic β-cells that naturally lack hypoglycemia/hypoxia inducible mitochondrial protein 1 (HIMP1) are susceptible to hypoglycemia and hypoxia influences. A linkage between the hypoglycemia/hypoxia susceptibility and the lack of HIMP1 is suggested in a recent study using transformed β-cells lines. To further illuminate this linkage, we applied mouse insulin 1 gene promoter (MIP) to control HIMP1-a isoform cDNA and have generated three lines (L1 to L3) of heterozygous HIMP1 transgenic (Tg) mice by breeding of three founders with C57BL/6J mice.

Desmoplakin is essential in epidermal sheet formation.

We have generated an epidermis-specific desmoplakin (DP) mouse knockout, and show that epidermal integrity requires DP; mechanical stresses to DP-null skin cause intercellular separations. The number of epidermal desmosomes in DP-null skin is similar to wild type (WT), but they lack keratin filaments, which compromise their function. DP-null keratinocytes have few desmosomes in vitro, and are unable to undergo actin reorganization and membrane sealing during epithelial sheet formation.

Hyperproliferation and defects in epithelial polarity upon conditional ablation of alpha-catenin in skin.

When surface epithelium was conditionally targeted for ablation of alpha-catenin, hair follicle development was blocked and epidermal morphogenesis was dramatically affected, with defects in adherens junction formation, intercellular adhesion, and epithelial polarity. Differentiation occurred, but epidermis displayed hyperproliferation, suprabasal mitoses, and multinucleated cells. In vitro, alpha-catenin null keratinocytes were poorly contact inhibited and grew rapidly.

Defining the regulatory factors required for epidermal gene expression.

Keratins K5 and K14 are the hallmarks of mitotically active keratinocytes of stratified epithelia. They are transcribed at a high level and in a tissue-specific manner, enabling us to use the K14 gene to elucidate the regulatory mechanism underlying epidermis-specific transcription. We have identified four DNase I-hypersensitive sites (HSs) present in the 5' regulatory sequences of the K14 gene under specific conditions where the gene is actively expressed.

The magical touch: genome targeting in epidermal stem cells induced by tamoxifen application to mouse skin.

Gene knockout technology has provided a powerful tool for functional analyses of genes expressed preferentially in a particular tissue. Given marked similarities between human and mouse skin, such studies with epidermally expressed genes have often provided valuable insights into human genetic skin disorders. Efficient silencing of a specified gene in a temporally regulated and epidermal-specific fashion could extend functional analyses to broadly expressed genes and increase the categories of human skin disorders to which parallels could be drawn.

FGF-7 modulates ureteric bud growth and nephron number in the developing kidney.

The importance of proportioning kidney size to body volume was established by clinical studies which demonstrated that in-born defecits of nephron number predispose the kidney to disease. As the kidney develops, the expanding ureteric bud or renal collecting system induces surrounding metanephric mesenchyme to proliferate and differentiate into nephrons. Thus, it is likely that nephron number is related to ureteric bud growth.

Desmoplakin is required early in development for assembly of desmosomes and cytoskeletal linkage.

Desmosomes first assemble in the E3.5 mouse trophectoderm, concomitant with establishment of epithelial polarity and appearance of a blastocoel cavity. Throughout development, they increase in size and number and are especially abundant in epidermis and heart muscle.

De Novo hair follicle morphogenesis and hair tumors in mice expressing a truncated beta-catenin in skin.

An effector of intercellular adhesion, beta-catenin also functions in Wnt signaling, associating with Lef-1/Tcf DNA-binding proteins to form a transcription factor. We report that this pathway operates in keratinocytes and that mice expressing a stabilized beta-catenin controlled by an epidermal promoter undergo a process resembling de novo hair morphogenesis. The new follicles formed sebaceous glands and dermal papilla, normally established only in embryogenesis.

The ovo gene required for cuticle formation and oogenesis in flies is involved in hair formation and spermatogenesis in mice.

The Drosophila svb/ovo gene gives rise to differentially expressed transcripts encoding a zinc finger protein. svb/ovo has two distinct genetic functions: shavenbaby (svb) is required for proper formation of extracellular projections that are produced by certain epidermal cells in late-stage differentiation; ovo is required for survival and differentiation of female germ cells. We cloned a mouse gene, movo1 encoding a nuclear transcription factor that is highly similar to its fly counterpart in its zinc-finger sequences.

Lymphadenopathy, splenomegaly, and altered immunoglobulin production in BCL3 transgenic mice.

The candidate proto-oncogene BCL3 was isolated through its involvement in the t(14;19) found in chronic lymphocytic leukemia and other B-cell neoplasms. As a member of the I kappaB family, BCL3 plays a role in the immune response by interactions with the NF-kappaB family of transcription factors. In order to study the role of BCL3 overexpression in lymphoid malignancies, we generated five lines of E mu-BCL3 transgenic mice.

Progressive kidney degeneration in mice lacking tensin.

Tensin is a focal adhesion phosphoprotein that binds to F-actin and contains a functional Src homology 2 domain. To explore the biological functions of tensin, we cloned the mouse tensin gene, determined its program of expression, and used gene targeting to generate mice lacking tensin. Even though tensin is expressed in many different tissues during embryogenesis, tensin null mice developed normally and appeared healthy postnatally for at least several months.

Keratinocyte growth factor is required for hair development but not for wound healing.

Keratinocyte growth factor (KGF), also known as fibroblast growth factor 7 (FGF7), is synthesized by skin fibroblasts. However, its mitogenic activity is on skin keratinocytes, where it is the most potent growth factor identified thus far. To explore KGF's function in vivo, we used embryonic stem cell technology to generate mice lacking KGF.

The basal keratin network of stratified squamous epithelia: defining K15 function in the absence of K14.

Keratin 5 and keratin 14 have been touted as the hallmarks of the basal keratin networks of all stratified squamous epithelia. Absence of K14 gives rise to epidermolysis bullosa simplex, a human blistering skin disorder involving cytolysis in the basal layer of epidermis. To address the puzzling question of why this disease is primarily manifested in skin rather than other stratified squamous epithelia, we ablated the K14 gene in mice and examined various tissues expressing this gene.

Gene targeting of BPAG1: abnormalities in mechanical strength and cell migration in stratified epithelia and neurologic degeneration.

BPAG1 is the major antigenic determinant of autoimmune sera of bullous pemphigoid (BP) patients. It is made by stratified squamous epithelia, where it localizes to the inner surface of specialized integrin-mediated adherens junctions (hemidesmosomes). To explore the function of BPAG1 and its relation to BP, we targeted the removal of the BPAG1 gene in mice.

Genetic bases of epidermolysis bullosa simplex and epidermolytic hyperkeratosis.

Keratins are the major structural proteins of the epidermis. Analyzing keratin gene sequences, appreciating the switch in keratin gene expression that takes place as epidermal cells commit to terminally differentiate, and elucidating how keratins assemble into 10-nm filaments have provided the foundation that has led to the discoveries of the genetic bases of two major classes of human skin diseases. In this report, we review the cell biology and human genetics of these diseases, epidermolysis bullosa simplex and epidermolytic hyperkeratosis.

Interleukin 6: insights to its function in skin by overexpression in transgenic mice.

Interleukin 6 (IL-6) is a cytokine that mediates a wide range of inflammatory and immune responses. Its expression is elevated in inflammatory or immunodeficient diseases, including psoriasis, rheumatoid arthritis, and AIDS. To explore the role of IL-6 in skin, we utilized a human keratin 14 (K14) promoter to express IL-6 in the basal cells of stratified squamous epithelia of transgenic mice.

Expression of v-src in embryonic neural retina alters cell adhesion, inhibits histogenesis, and prevents induction of glutamine synthetase.

Using Rous sarcoma virus as the vector, v-src or c-src genes were introduced into 6-day chicken embryo retina tissue in organ culture and their effects on retina development were investigated. Overexpression of c-src in many of the cells had no noticeable effect on retina development. In contrast, infection with v-src resulted in abnormal histogenesis and inhibition of differentiation.

Mutant keratin expression in transgenic mice causes marked abnormalities resembling a human genetic skin disease.

To explore the relationship between keratin gene mutations and genetic disease, we made transgenic mice expressing a mutant keratin in the basal layer of their stratified squamous epithelia. These mice exhibited abnormalities in epidermal architecture and often died prematurely. Blistering occurred easily, and basal cell cytolysis was evidence at the light and electron microscopy levels.

Embryonic cell recognition: uncoupling tissue-specific affinities from cell-type specificities.

We have experimentally defined the two major aspects of embryonic cell recognition-adhesion (ReAd), tissue type-specific ReAd and cell type-specific ReAd; we showed that they arise consecutively during cell differentiation, and that the former can function in the absence of the latter. Embryonic chick cells (retina and chondroblasts) in which differentiation was arrested by BrdU at an early stage, failed to express cell-type ReAd, yet they continued to display tissue-type ReAd: they distinguished tissue-self from non-self and selectively cohered with self. Our results indicate that tissue-type and cell-type ReAd represent distinct, separately controlled mechanisms.

Cell contacts are required for induction by cortisol of glutamine synthetase gene transcription in the retina.

In embryonic neural retina the enzyme glutamine synthetase [GS; L-glutamate:ammonia ligase (ADP-forming), EC 6.3.1.

Retinoic acid inhibits conversion of dissociated Müller glia into lens-like cells.

In monolayer cultures of dissociated retina cells, Müller gliocytes undergo conversion into a lens-like cell type (lentoidal cells): they become unable to adhere to neurons and accumulate lens antigens. Retinoic acid (RA) retards these changes. We present evidence that RA prevents the rapid loss of gliocyte adhesivity to neurons; and that, by promoting restoration of glia cell contacts with neurons, RA protects the gliocytes from phenotype alteration.

Antiserum to lens antigens immunostains Müller glia cells in the neural retina.

Antiserum to a lens fraction enriched for alpha-crystallin selectively immunostains Müller glia cells in the neural retina of several vertebrate species. Also, in embryonic retina (chicken), this antiserum reacts with Müller cells and, at early stages of development, with their apparent precursors. Thus, antibodies to a lens product(s) detect a Müller glia cell marker that begins to be expressed very early in their ontogeny and can be useful in studies on differentiation, function, and pathologies of this cell type.

Transformation of retinal glia cells into lens phenotype: expression of MP26, a lens plasma membrane antigen.

We describe experiments in which dissociated cells from differentiated, post-mitotic neural retina of late chicken embryos (13 and 16 days) rapidly and consistently transform (transdifferentiate) in vitro into lens-like phenotype and form spherical lentoids. Using immunohistochemical and other tests, we have established that the lentoids arise from the progeny of definitive retinal glia cells (Müller cells). An early event in their transformation is the appearance in the cell surface of MP26, a plasma membrane protein characteristic of lens but not found in the retina.